here - Australian College of Veterinary Scientists

Australian College of Veterinary 

Scientists Dermatology Chapter 

Science Week Proceedings 2005 

Equine Dermatology 

ACVSC Proceedings Dermatology Chapter Science Week 2005 1

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ACVSc Dermatology Chapter 

This is the third Science Week meeting of our Dermatology Chapter and 

we are looking forward to an exciting two days of equine dermatology. 

We are very pleased to welcome our key-note speakers Dr Janet 

Littlewood and Dr Reg Pascoe as well as Australian and European 

dermatologists, dermatology residents and pathologists who have all 

combined to create a fabulous program for dermatologists as well as 

equine clinicians for Science Week 2005. 

This continues to be an important time for veterinary dermatology in 

Australia. The Dermatology Chapter aims promote excellence in 

dermatology of all animal species. The objectives of the Chapter include 

advancing the science and art of veterinary science as it relates to 

dermatology and in particular to further the professional education and 

training of veterinarians with a special interest in dermatology. 

For further information on joining the Dermatology Chapter, please 

contact Mandy Burrows on a.burrows@murdoch.edu.au. 

ACVSC Proceedings Dermatology Chapter Science Week 2005

Australian College of Veterinary Scientists Dermatology Chapter 


Friday 1st July 2005 : Equine dermatology: Program 

8.20 Introduction: Equine allergic skin disease 

Mandy Burrows 

8.30 Equine atopic skin disease 

Janet Littlewood 

9.10 Intradermal testing in horses: the Australian perspective 

Tina Baxter 

10.00 Morning tea 

10.30 Intradermal testing in horses: the UK perspective 


11.10 Equine Rhodes grass contact allergy 

Ken Mason 

11.30 Immunotherapy for equine atopy 


12.30 Lunch 

1.30 Diagnostic approach to the horse with urticaria 

Reg Pascoe 

2.30 Urticaria case studies 

Greg Burton 

3.00 Afternoon tea 

3.30 Management of the atopic horse 


4.30 Dermatology AGM 


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Australian College of Veterinary Scientists Dermatology Chapter 


Saturday 2nd July 2005 : Equine Dermatology (cont) 

8.20 Introduction: Equine dermatology 

Mandy Burrows 

8.30 The approach to the horse with pastern dermatoses 


9.20 A review of equine sarcoidosis 

Sonya Bettenay 

10.00 Morning tea 

10.30 The equine sarcoid: a review 

Reg Pascoe 

11.50 Histopathologic features of equine sarcoid 

Jenny Charles 

12.30 Lunch 

1.30 How I treat: equine bacterial folliculitis 


1.50 How I treat: equine insect hypersensitivity 

Mandy Burrows 

2.10 How I treat: equine pemphigus foliaceus 

Ralf Mueller 

2.30 How I treat: equine phycomycoses 

Reg Pascoe 


3.00 Afternoon tea 

3.30 How I treat: equine dermatophytosis 

Greg Burton 

3.50 How I treat: equine chorioptes 


4.10 How I treat: equine vasculitis 

Linda Vogelnest 

4.30 CLOSE 


Dr Tina Baxter 

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About the speakers: 

Graduated from University of Sydney in 1999 

- Worked in busy small animal practice after graduating 

- Did distance education course in Derm with Ralf and Sonya in 2003 

- Virbac created position for Resident in Derm at Sydney Uni through 

generous grant 

- Started this residency in 2004 

- Passed membership exams in Small Animal Med in 2004 

- Derm interests - any equine dermatology - research project into allergen 

concentration determination in horses. 

Dr Sonya Bettenay BVSc (Hons) MACVSc (Feline Medicine) FACVSc 

(Dermatology) 

Graduated from Melbourne University, worked in private small animal practice, 

industry and teaching Vet Nurses and Equine courses during the first 8 years of 

graduation and then began a residency with Dr Ken Mason. Coinciding with this, 

founded the Animal Skin & Allergy Clinic in Melbourne, with satellite clinics in 4 

States until we obtained enough dermatologists to cover Adelaide, Canberra and 

Sydney. With her husband, Ralf Mueller, built the first purpose built private 

dermatology clinic in Australia. She is currently employed at Colorado State 

University and runs the dermatopathology service of the CSU Diagnostic Lab. 

Dr Mandy Burrows BVMS MACVSc (Canine Medicine) FACVSc 

(Dermatology) 

Graduated from Murdoch University in 1985. Completed a pathology and small 

animal residency at Murdoch University and Membership in Canine Medicine in 

1991. Commenced a dermatology residency in 1992 with Ken Mason and gained her 

Fellowship in Veterinary Dermatology in 1998. Mandy currently runs a dermatology 

referral practice at Murdoch University Veterinary Hospital and teaches dermatology 

and immunology to undergraduate and postgraduate veterinary students and has a 

strong interest in continuing veterinary education for veterinary practitioners and 

nurses. 

Dr Greg Burton 

Graduated University of Queensland (Hons 1st) 1983 

Small animal general practice 1983-1993 

Member ACVSc (small animal surgery) 1993 

Fellow ACVSc (dermatology) 1997 

Currently in referral dermatology practice Melbourne Veterinary Referral Centre and 

University of Melbourne Veterinary Teaching Hospital, Melbourne 

Principal Fellow (Associate Professor), Dept of Veterinary Science, University of 

Melbourne 3010 


Dr Jennifer A. Charles BVSc MVS Dip ACVP 

Jenny Charles graduated from The University of Sydney in 1985. She completed an 

internship, residency and Master of Veterinary Studies in anatomic pathology at The 

University of Melbourne and then pursued advanced studies in anatomic pathology 

at the Ontario Veterinary College, Guelph, Canada. In 1993, she became a 

Diplomate of the American College of Veterinary Pathologists. From 1993 to 1999, 

she was employed as a specialist veterinary pathologist at the Sydney Laboratory of 

Veterinary Pathology Services Pty Ltd (now IDEXX Pty Ltd). In 1999, she was 

appointed Senior Lecturer in Veterinary Pathology at The University of Melbourne. 

Jenny’s particular interests lie in haematology, endocrinology, hepatobiliary and 

pancreatic pathology and dermatopathology. 

Dr Janet Littlewood MA PhD BVSc (Hons) DVR DVD MRCVS RCVS 

Recognised Specialist in Veterinary Dermatology 

Janet graduated with Honours from the University of Bristol, longer ago than she 

cares to remember! As a new graduate she spent a year as Intern at the University of 

Pennsylvania, she spent some time in general practice before being appointed 

Assistant Physician at the University of Cambridge. After this training in small 

animal medicine, she studied for her PhD in aspects of comparative haemostasis, but 

then returned to clinical medicine and to focus on dermatology. She established the 

Dermatology Unit at the Animal Health Trust, Newmarket, where she developed her 

interest in equine dermatology, in addition to the small animal clinical work, training 

residents and supervising a research student working on canine atopy. She holds the 

RCVS Diploma and has Recognised Specialist status in Veterinary Dermatology and 

has been examiner for both Certificate and Diploma examinations. She has written 

chapters for and edited a number of textbooks as well as contributing to peer 

reviewed journals. She is involved in postgraduate continuing education and has 

spoken at many national and international conferences and is renowned for her 

enthusiasm for her subject. Since 2001 Janet has been working in private referral 

practice in East Anglia, offering a service for companion animals, including horses. 

As well as running her business, Janet is mum to two sons, is overseeing major house 

renovations, and still tries to find time to sing with the Cambridge Philharmonic 

Society and is learning to play the viola. 

Dr Ken Mason BSc BVSc MVSc MACVSc (Feline Medicine) FACVSc 

(Veterinary Dermatology) 

Clinical veterinarian, animal dermatologist and by marriage a cat person. 


Dr. med. vet. Ralf S Mueller 

Graduated in Munich/Germany in 1985, completed his thesis in 1987, and worked in 

several large and small animal practices before completing a residency in veterinary 

dermatology at the University of California/Davis in 1992. He is a Diplomate of the 

American College of Veterinary Dermatology and a Fellow of the Australian College 

of Veterinary Science. In 1992 he moved to Melbourne/Australia to work with his 

partner and wife Dr. Sonya Bettenay. Together, they created the first, purpose-built 

specialist practice not linked to a general practice in Australia. They established the 

Distance Education Program in Veterinary Dermatology of the Postgraduate 

Foundation in Veterinary Science of the University of Sydney. During that time, Dr. 

Mueller was concurrently consulting and teaching at the Veterinary Teaching 

Hospital/University of Sydney. In 1999, he became Assistant Professor in Veterinary 

Dermatology at the College of Veterinary Medicine and Biomedical 

Sciences/Colorado State University, where he is involved in teaching, consulting and 

veterinary dermatology research. He has published over 100 studies, articles, book 

chapters and books in the German, English, Spanish and French literature in 

Australia, Europe and America and given over 200 seminars, lectures and talks in 

Australia, Europe, United States, New Zealand and Canada. Dr. Mueller has two 

children, Anya and Florian and when he is not working, he takes his family skiing, 

rock-climbing or hiking. 

Dr Reg Pascoe AM, BVSc. DVSc. FRCVS. FACVSc. 

Graduated from the University of Queensland in 1951. Commenced general large 

animal practice in Oakey and in 1969 established a large animal hospital, 

predominantly for horses. Is a registered specialist in Equine Surgery and has a 

special interest in Dermatology, presenting his first paper on skin diseases in 

1971.Author and co author on four equine Dermatology books and over 60 

refereed scientific published articles 

Biography: University of Queensland BVSc 1951, MVSc. 1967 , DVSc. 1984; 

Adjunct Professor Veterinary Science 1998; FRCVS 1973, FACVSc 1975. Began 

private general rural practice in Oakey 1952; equine practice covering reproduction, 

surgery and dermatology from 1966; Specialist in Equine Surgery since 1988. 

Published over 60 referred articles, author of Equine Dermatoses (3 editions), 

Colour Atlas of Skin Diseases of Horses, and Vade Mecum II - Diseases of 

Horses.Co-author Colour Atlas of Equine Diseases and Handbook of Equine 

Dermatology. 

Dr Linda Vogelnest 

Graduated from Sydney University 1984. Worked in small animal practice in 

Australia and locuming in UK for 4 years. Full-time head of small animal unit at 

Sydney University Veterinary Centre Camden for 2 years, then part-time registrar in 

small animals for 8 years. Achieved Membership of Australian College of Veterinary 

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Scientists in Feline Medicine in 1997. Completed Dermatology Alternative Residency 

Program, supervised by Ralf Mueller, Ken Mason, Sonya Bettenay, Greg Burton, 

from 1997-2001; 3 years based in Sydney, one year in Melbourne. Achieved 

Fellowship of Australian College of Veterinary Scientists in Veterinary Dermatology 

in 2003. Currently employed as Specialist Veterinary Dermatology at University of 

Sydney (Camden campus 3 days, Sydney campus 1 day per week) seeing small, large 

and exotic animal referrals. 


Introduction: 

10 

Equine Atopic Dermatitis 

ACVSC Proceedings Dermatology Chapter Science Week 2005 


Atopic dermatitis is defined as a genetically programmed disease mediated by 

reaginic-antibodies (type I hypersensitivity) in which the patient becomes sensitised 

to environmental allergens that are innocuous for non-atopic animals. Classically the 

diseases is associated with IgE allergen-specific antibodies, but in some species 

evidence supports a role for allergen-specific IgG. The importance of other 

components of the immune system are now known to be important in the aetiology 

of the disease process. 

In humans and dogs there is good evidence that the disease is genetically 

programmed and there are reports of familial incidence and breed predispositions in 

the horse that suggest genetic involvement. It is well recognised that insect bite 

hypersensitivity (IBH, Culicoides hypersensitivity) has a strong familial tendency, and 

there are reports of familial occurrence of equine atopy suggesting a genetic 

predisposition (Rees 2001). Factors such as susceptibility to sensitisation during early 

life and the influence of the presence of parasitic infestation, viral infections, 

vaccination and environmental pollutants are of unknown significance in the horse. 

Genetically-predisposed individuals mount allergen-specific IgE (and possibly IgG) 

antibody responses to environmental (and possibly ingested) antigens. Equine IgE 

was isolated and characterised by Suter and colleagues in the early 1980's, with even 

earlier documentation of skin-sensitising antibodies. IgE binds to mast cells in the 

skin (and elsewhere) via the high-affinity IgE receptor. Cross-linking of mast cellbound 

IgE by specific allergens, causes degranulation and release of preformed 

mediators, giving rise to the classical erythematous wheal reaction, and synthesis of 

new mediators resulting in the recruitment of inflammatory cells to the area. 

However, the lesions that develop in atopic humans and dogs at the site of patch 

tests more closely mimic those found in the naturally occurring clinical disease. 

Atopic individuals show increased numbers of both dermal and epidermal 

Langerhans cells, as well as increased numbers of other inflammatory cells. 

Epidermal Langerhans cells have been shown to bear allergen-specific IgE molecules 

in atopic humans and dogs, further supporting that percutaneous absorption of 

allergens is important in the aetiology of the natural disease, probably aided by 

epidermal barrier function defects.

IgE-bearing cells have been demonstrated in the epidermis and dermis of lesional 

skin from horses with IBH, together with increased numbers of mast cells, the 

majority of which were tryptase-positive (van der Haegen et al 2001) and also 

bearing IgE protein. No chymase-positive cells were found, similar to bovine skin, 

but in contrast to human and canine skin where mast cells are both chymase and 

tryptase-positive. IgE-mRNA and IgE-protein positive cells were found in the 

dermis – likely B-lymphocytes and plasma cells – but also IgE-protein positive, 

mRNA negative cells in both the dermis and the epidermis, which are likely to be 

dendritic cells, including Langerhans cells. By comparison with samples from healthy 

horses and horses with an infectious skin disease, this study was the first to provide 

evidence demonstrating the role of IgE in the skin of allergic horses. 

Epidermal Langerhans cells bearing IgE are thought to capture percutaneously 

absorbed allergen, process and present to allergen-specific T-lymphocytes. In atopic 

humans there is subsequent preferential expansion of T-helper cells of the Th2subset, 

which release cytokines such as interleukin (IL)-4, with resultant stimulation 

of IgE production by B-cells. The cytokine profile of the increased number of Tlymphocytes 

demonstrated in the skin of allergic horses has yet to be elucidated. 

The horse, in comparison to humans and dogs, shows a prominent late-phase 

component 4-6 hours after intradermal challenge. As well as IgE-cross-linking 

resulting in histamine release from mast cells, liberation of histamine from equine 

basophils has also been demonstrated. Increased concentrations of a numbers of 

inflammatory mediators has been documented during inflammatory reactions in the 

horse, including eicosanoids, lysosomal enzymes, proteases, IL-1, leukotriene (LT)B 4, 

prostaglandin (PG) E 2, histamine, serotonin, superoxides and tumour necrosis factor 

(TNF). 

In allergic skin disease in the horse the eosinophil is particularly important, together 

with histamine, LTB 4 and platelet aggregating factor (PAF). Histamine injected 

intradermally results in the ingress of numerous eosinophils and results in marked 

oedema. Injection of LTB 4 and PAF also stimulates migration of eosinophils and 

oedema, the number of eosinophils being proportional to the oedema. Foster and 

colleagues at the Royal Veterinary College, London, studied cutaneous inflammation 

in horses and demonstrated the importance of PAF and LTB 4 in horses with sweet 

itch (IBH). PAF and LTB 4 induction of migration of eosinophils and neutrophils in 

horses with allergic skin disease. PAF was shown to mimic antigen-induced 

inflammatory responses and receptor antagonists to inhibit the responses. 

Eosinophils are reported as the predominant inflammatory cells in skin biopsies 

taken from atopic horses, as well as those with IBH. Eosinophils contain a range of 

cytotoxic proteins and produce several potent inflammatory mediators and are 

pivotal in the inflammatory process triggered by hypersensitivity reactions in the 

horse. 


Clinical features: 

Whilst summer seasonal recurrent dermatitis has been long-recognised in the horse 

and the aetiopathological role of hypersensitivity responses to the bites of insects, 

particularly Culicoides species was elucidated as long ago as the early 1970's, the 

concept of equine atopy was later in becoming recognised, being featured in 

textbooks by the end of the 1980's. Although now universally recognised, the 

prevalence of equine atopic dermatitis is not known. Scott and Miller (2003) report 

atopy as the seventh most common equine dermatosis diagnosed at the Cornell 

University Clinic, accounting for 3.89% of all skin conditions, but some or all of an 

additional 2.11% with a final diagnosis of idiopathic pruritus and 2.44% with 

idiopathic urticaria might also be considered as atopic – giving a possible total of 

8.44% of horses with skin disease. 

Clinical signs most commonly begin in young horses, 1.5-6 years of age. There is no 

sex predilection, but some reports suggest breed predisposition, but there is not 

usually any comparison to a reference population to validate the observation(s). 

Signs may be seasonal or non-seasonal, depending upon the allergens involved, and 

may initially be seasonal and progressing to be perennial in nature. The major clinical 

signs in equine atopic dermatitis are pruritus and/or urticaria. Early in the course of 

the disease affected horses may present with pruritus without obvious 

dermatological lesions. Rubbing, biting, stamping, tail-flicking and, occasionally, head 

-shaking may be reported. Subsequent self-inflicted damage resulting in the presence 

of excoriations, partial to complete alopecia, lichenification, thickening and folding 

of the skin, hyperpigmentation and secondary bacterial infections. Affected areas 

included the head, ears, neck, trunk, and legs; in some cases there is also involvement 

of the regions classically affected in IBH – the dorsolateral neck, mane, dorsal 

midline lumbar area and tail base. Urticaria is also a common reaction pattern in 

atopic horses, sometimes seen in conjunction with pruritus, but in some cases being 

non-pruritic. Some atopic horses present with tufted papules or nodules, which may 

become crusted and alopecic. Biopsy of these lesions reveals the presence of 

eosinophilic folliculitis (sterile) and/or eosinophilic granulomata. 

Horses with atopic dermatitis are only rarely reported to show signs of concurrent 

allergic conjunctivitis, rhinitis and chronic obstructive pulmonary disease (COPD). 

Whilst there is evidence that COPD is an atopic disease (genetically driven, 

hypersensitivity response to environmental allergens causing clinical disease), reports 

of concurrent atopic dermatitis and COPD are rare. 

In a series of 24 horses referred to the author whilst at the Animal Health Trust, 

Newmarket, for investigation of clinical signs suggestive of an allergic aetiology, but 

not consistent with classical summer seasonal recurrent dermatitis due to insect-bite 

hypersensitivity, the history and presenting signs were analysed (Littlewood et al 

1998). Seven of the horses were thoroughbreds (TB) and a further eight were TBcrosses, 

with five Welsh cob, unspecified cobs or cob-crosses, one Arab, one Arabcross, 

one Belgian warmblood and one pony. Age at diagnosis ranged from 2-30 

12 


years, median age 6.5 years, with age of onset of disease 1-27 years (median 5.5 years) 

and duration of clinical signs at time of referral ranging from 2 months to >5years. 

Fourteen of the horses presented with pruritus and six with pruritus and urticaria. 

Four horses had recurrent or chronic urticaria without obvious pruritus, including 

one with angio-oedema. The degree of pruritus was considered to be severe in six 

animals, and was particularly severe in case 3 (see figure 1) resulting in self inflicted 

damage and requiring the use of a nosebag to prevent biting. In most cases the 

clinical signs were restricted to the trunk, with tail rubbing also present in seven, 

mane involvement in two and facial irritation noted occasionally. Papules or 

“bumps” were reported or found on dermatological examination in six cases. Two 

horses had histories of intercurrent respiratory problems thought to be of allergic 

aetiology on the basis of previous investigations (endoscopy and cytological 

examination of tracheo-bronchial washes). In 12 horses the clinical signs were 

perennial, with exacerbation in the summer noted in two and winter exacerbation in 

two others. Four animals showed a seasonal pattern to their skin problem, one of 

which was restricted to spring, two to the winter and the fourth to the summer. This 

latter horse was only stabled in the summer and turned out all winter. In eight 

animals the duration of clinical signs was not long enough to determine if the 

problem was going to be perennial, but in six the signs began in autumn or winter 

and two started with symptoms in late summer or autumn. All animals were stabled 

for at least 50% of the day, with 15 horses being stabled full time at the time of 

maximal clinical signs. 

Diagnosis: 

A large number of differential diagnoses may need to be considered, depending on 

the history and distribution of clinical signs, but would include: 

insect hypersensitivity 

ectoparasites (lice, chorioptic mange, psoroptic mange, trombiculidiasis, 

poultry mites) 

oxyuriasis 

forage/storage mites 

helminth infestations (oxyuriasis, strongyloidosis, Pelodera cutaneous larval 

migrans) 

contact dermatitis 

adverse cutaneous food reaction 

drug reactions 

systemic diseases causing pruritus (rare cases of lymphoma, hepatic and renal 

neoplasia) 

As in the dog and cat, the diagnosis of atopic dermatitis is reached after ruling out all 

other possible differentials and the diagnosis is essentially a clinical diagnosis. 

Laboratory investigations such as routine haematological and biochemical profiles 

are rarely contributory to reaching a diagnosis in atopic horses, but may be indicated 

to investigate possible systemic disease in cases with suggestive clinical signs. Skin 


iopsies may offer supportive evidence, the typical histopathological features being 

superficial to deep, perivascular to interstitial dermatitis with eosinophils being the 

predominant inflammatory cell. The epidermis is often hyperplastic. Spongiosis and 

dermal oedema may be seen. Eosinophilic mural folliculitis and eosinophilic 

granulomata may occasionally be present as focal changes. These changes are not 

pathognomonic for equine atopy and may be present in other hypersensitivity 

disorders such as IBH. 

Once a clinical diagnosis is reached, specific allergy testing may be employed to 

identify allergens that may be implicated in the individual patient so that avoidance 

strategies or immunotherapy can be formulated. 

Specific allergy testing: 

Classically identification of implicated allergens in allergic patients has employed 

intradermal testing. Studies documenting optimal testing procedures for the horse 

are limited and comparisons between different commercial sources of allergens are 

difficult, since it has been shown the bioactivity of products may vary form 10- to 

1000- fold, with no relationship between bioactivity and declared concentrations. 

There is little published about threshold concentrations of various allergens for the 

horse, to try and avoid false-positive, irritant reactions in non-allergic horses. There 

are problems of standardisation of allergen extracts in terms of the source, raw 

material, extraction methods, identification of substances, standardisation of 

concentration of ingredients, stabilisation and potency. Selection of allergens for 

testing should take account of the experience of colleagues in the human and 

veterinary field, preferably those working in the same region. Use of allergen mixes is 

not advised, in case of false-negative reactions in horses allergic to only one or two 

of the mix – although the presence of common allergens within certain groups of 

allergens, particularly tree pollens and grass pollens, may make this of less concern. 

Moulds and weed pollens show less antigenic similarity and thus testing with 

individual allergens is of more importance in these groups. 

False positive skin test reactions have been reported by a number of investigators. 

Fadok (1986) tested 39 normal horses and documented false positive reactions, 

mostly to insects, with more reactions in horses over 6 years of age; no false positive 

reactions were found with pollens or mould extracts. Evans et al (1992) reported 

false positives in a study of horses with COPD and urticaria, which were thought to 

be possibly subclinical cases. Interestingly, intradermal tests performed on specificpathogen 

(parasite) free ponies gave no positive reactions (Foil 1992). 

Rosenkrantz et al (1998) studied 28 horses with IBH and atopic disease and ten 

normal horses. Three of the ten had no reactions, but seven showed positive 

reactions, three including delayed reactions, against 1-9 antigens. Insect reactions 

were commonly found in these normal horses (deer fly, horse fly, house fly, black 

fly, mosquito, flea) and also weeds (yellow dock, Russian thistle, firebush). Other 

allergens that have been suggested to be possible irritants in horses include grain mill 

14 


dusts, grain smuts, moulds, danders and mites and so positive reactions must be 

interpreted with caution. 

More recent studies of intradermal testing in horses with atopic dermatitis or 

recurrent urticaria, compared to non-atopic horses, revealed significantly greater 

mean numbers of positive reactions in horses with skin disease, at 30minutes 

(immediate) and late-immediate and delayed time points, and to significantly higher 

numbers of allergens in each group of allergens (Lorch et al 2001, Jose-Cunilleras et 

al 2001). The authors emphasise that the presence of positive reactions to individual 

allergens is not diagnostic of hypersensitivity, but patterns of reactivity are helpful in 

management of cases when used together compatible history and evidence of 

exposure. 

Selection of strict criteria for interpretation of positive versus negative results has 

been shown to reduce the number of false positive or irrelevant results and improve 

the sensitivity and predictive value of intradermal testing (Jose-Cunilleras et al 2001). 

Wheal reactions should be scored on the basis of diameter and turgidity of the 

reaction, in comparison to the controls. However, there is no consensus on the 

criteria for scoring: a scale of 0-5+ is commonly cited, where 0 is the size of the 

negative control, 5+ is the maximal response, 4+ is the size of the histamine control 

and 2+ is the mean of the difference between the positive and negative controls. 

Whilst 2+ reactions and greater have been considered positive by many authors, 

using a cut-off of 3+ and greater reactions is recommended. 

In summary, a “positive” skin test reaction may indicate clinically relevant 

hypersensitivity, subclinical hypersensitivity or an irritant, false-positive reaction. 

Normal horses often show positive reactions, particularly to insect extracts, and 

show increasing numbers of positive reactions with age. Nonetheless, in horses with 

compatible clinical signs, intradermal testing is extremely useful in case management. 

Serological testing to identify the presence of circulating, antigen-specific IgE has 

received much attention in human and canine atopic disease, with fewer publications 

in feline and equine allergic skin disease. A number of problems exist with these in 

vitro tests, including the fact that IgE titres in dogs do not correlate with clinical 

disease. Heterogeneity of IgE is thought to exist, with some types being associated 

with clinical disease (IgE+) and others not (IgE-). Alternatively the defect may be 

at target tissue level rather than in circulating IgE concentrations. Studies at the 

Animal Health Trust with various reagents employed in canine in vitro tests, and 

published studies, have shown marked variation in test results with different 

reagents. Samples sent to different commercial companies have shown poor 

reproducibility of results. Normal dogs and dogs with any kind of skin disease may 

show positive reactions and publications have shown poor to moderate correlation 

with intradermal testing in dogs and cats. Some of these findings may be explained 

by poor specificity – particularly with polyclonal anti-IgE, but also with some 

monoclonal, reagents cross-reacting with other classes of immunoglobulin; low 


affinity of binding with monoclonal reagents may also be a problem. Species 

specificity of reagents is also of vital importance. 

The most recent technology employs a recombinant peptide of the alpha chain of 

the high-affinity Fc epsilon receptor for detection of IgE (Allercept reagent), and has 

vastly improved specificity. Studies of more than 250 atopic dogs comparing 

intradermal testing with Greer allergens and Allercept serological test results showed 

good correlation for dogs with housedust mite sensitivity, although intradermal 

testing was more sensitive; insufficient data were available to analyse other allergens 

(Foster et al, 2003). 

In the horse various commercial tests are available, but there is little published 

evidence concerning the validation and reliability of such tests. A test using the 

FcR1 -based assay for horses is now available and there is some published data 

comparing this and other in vitro tests with intradermal tests (Lorch et al 2001). 

Seventeen horses with recurrent urticaria and/or atopic dermatitis, 16 with COPD 

and 22 non-atopic horses were studied with a panel of 73 intradermal antigens and 3 

serological tests. The test using the FcR1 -based assay had the overall highest kappa 

statistic positive predictive and negative predictive values, but overall agreement with 

the intradermal test was only fair. The highest kappa statistic was for horses with 

atopic dermatitis. The kappa statistics for the radioallergosorbent test (RAST) and a 

polyclonal-base ELISA agreed only slightly with that of the intradermal test. The 

authors concluded that none of the three serum tests reliably detected allergen 

hypersensitivity, compared to the intradermal test, although the FcR1 -based assay 

performed significantly better than the other two tests, but the low sensitivity of all 3 

assays indicated the need for more sensitive tests. 

Antisera have been raised against equine epsilon chain peptides, derived from the 

nucleotide sequence of equine IgE and one reagent was found to be useful in the 

detection of equine IgE in clinically allergic animals and also as a research tool 

(Kaline et al 2003). 

Whilst the serological tests offer the clinician the attraction of an easily performed 

test, the shortcomings of the currently available tests are considered by Scott and 

Miller (2003) “to be of no diagnostic or therapeutic benefit and to be a waste of 

money” 

16 


References: 

Evans AG, Paradis MR, & O'Callaghan M. (1992) Intradermal testing of horses with 

chronic obstructive pulmonary disease and urticaria. American Journal of Veterinary 

Research53, 203 

Fadok V (1986) Equine pruritus: results of intradermal skin testing. Proceedings of the 

Annual Meeting of the American Academy and College of Veterinary Dermatology New 

Orleans, p6 

Foil C (1992) Therapy of equine pruritus. Proceedings of the 2 nd World Congress of 

Veterinary Dermatology, Montreal, Canada p434 

Foster AP, Littlewood JD, Webb P, Wood JLN, Rogers K & Shaw SE. (2003) 

Comparison of intradermal and serum testing for allergen-specific IgE using a 

FcR1 -based assay in atopic dogs in the UK. Veterinary Immunology & 

Immunopathology 92, 51-60 

Jose-Cunilleras E, Kohn CW, Hillier A, Saville WJ & Lorch G. (2001) Intradermal 

testing in health horses and horses wih chronic obstructive pulmonary disease, 

recurrent urticaria, or allergic dermatitis.Journal of the American Veterinary Medical 

Association 219, 1115-21 

Kalina WV, Pettigrew HD & Gershwin LJ (2003) IgE ELISA using antisera derived 

from epsilon chain antigenic peptides detects allergen-specific IgE in allergic horses. 

Veterinary Immunology & Immunopathology 92, 134-47. 

Littlewood JD, Paterson S, & Shaw SC. (1998) Atopy-like skin disease in the horse. 

Advances in Veterinary Dermatology 3, p563 

Lorch G, Hiller A, Kwochka KW, Saville WA & LeRoy BE (2001) Results of 

intradermal tests in horses without atopy and with atopic dermatitis or recurrent 

urticaria. American Journal of Veterinary Research 62, 1051-9 

Rees CA (2001) Response to immunotherapy in six related horses with urticaria 

secondary to atopy. Journal of the American Veterinary Medical Association 218, 753-5 

Rosenkrantz WS, Griffin CE, Esch RE & Mullens BA (1998) Responses in horses to 

intradermal challenge of insects and environmental allergens with specific 

immunotherapy. Advances in Veterinary Dermatology 3, 191-200 

Scott DW & Miller WH (2003) Skin immune system and allergic skin diseases. In 

Equine Dermatology, Elsevier Science pp395-474. 

Van der Haegen A, Griot-Wenk M, Welle M, Busatro A, von Tscharner C, 

Zurbriggen A & Marti E (2001) Immunoglobulin-E-bearing cells in skin biopsies of 

horses with insect bite hypersensitivity. Equine Veterinary journal 33, 699-706 


18 

Intradermal Testing (IDT) in Horses: 

The Australian Perspective 

Applications of IDT in Australia 


Tina Baxter 

Intradermal testing (IDT) is probably an underutilized diagnostic tool in Australia. 

The incidence of atopy in Australian horses has not been documented. ‘Skin disease’ 

or ‘itch’ is a common presentation - approximately 20% of horse owners surveyed 

recently in Queensland reported their horses had a ‘skin problem’ (28) - and the 

majority of these had clinical presentations that were consistent with insect bite 

hypersensitivity. As the exact trigger of the skin disease was not identified in these 

cases, there may be a poor clinical distinction between insect related hypersensitivity 

and atopic dermatitis. 

More importantly, intradermal testing has applications in diseases other than atopic 

dermatitis, both here and overseas, and the following notes are equally relevant in 

performing the test for horses with insect bite hypersensitivity (including Queensland 

itch), recurrent urticaria, head shaking, chronic obstructive pulmonary disease and 

other airway diseases (reactive airway disease) where an allergic basis is suspected 

(7,12, 14, 16, 25). While Type I hypersensitivity is not the only contributing factor in 

these diseases, information gained from intradermal testing in these cases can only be 

of benefit. In a survey of aged horses, an estimate of 22% of horses had respiratory 

disease and the majority of these are thought to have an allergic pathogenesis (28). 

Possible reasons for the relative paucity of equine cases undergoing intradermal 

allergy testing include: 

The test requires time, skill and experience to perform, such that it is usually 

performed only by specialists in dermatology 

Much of the information and experience in IDT available to specialists in 

dermatology is based on small animals. Clinic facilities and personal 

preference of the dermatologist may preclude the handling of horses 

The allergens used in the test have a limited shelf life, so regular tests need to 

be performed to make the purchase of the allergens worthwhile and ensure 

the cost of the test to the individual owner remains reasonable 

Referral requires effort on the owners part to travel (in some cases significant 

distances from country regions of Australia) to the nearest major centre 

Costs and time to the owner: the average cost to the owner for IDT and 

consultation are around$500 to $650; costs of travel and time are additional

Comparatively simple, cheap and effective treatments are offered by the 

general veterinarian. Glucocorticoids, environmental management (such as 

stabling, rugging, topical insecticides), antibiotics and antihistamines are 

often prescribed, with many patients achieving acceptable control of their 

clinical signs with this management. 

Additional treatment options made available by results of IDT may be 

perceived to be more complex and expensive; allergen specific 

immunotherapy (ASIT) is an onerous task for many owners despite it’s 

benefits; and avoidance of allergens is usually impractical or impossible. 

Lack of awareness by horse owners that allergy testing is available and offers 

a beneficial alternative or adjunct to other standard treatments 

Often cases are referred as a last resort and poorer results are attained than 

had the case been referred early in the course of disease 

Education of both horse owners and veterinarians of the availability of IDT, and its 

means to improved management of many affected patients, is essential to improve the 

utilization of intradermal allergy testing as a diagnostic tool. 

Availablility of IDT in Australia 

There are only four centres in Australia at which equine intradermal testing is 

performed in Australia: 

Sydney 

Melbourne 

Perth 

Brisbane 

Following are the summarized details of the testing procedure, which for the most 

part, are similar across the different centres. 

Allergen Purchase 

For all four centres, allergen extracts are purchased through Dermcare Vet (Pty Ltd) 

who import the extracts from Greer Laboratories (Lenoir NC, USA). 

Allergen Selection 

Each centre has selected a range of allergens based on regional knowledge of relevant 

plants and insects, but is somewhat limited by the allergens available from the 

manufacturer. Allergen selection can be refined through various sources of 

information: 

Physicians in human allergy (and allergen testing panels from the same 

geographical region) 

National pollen charts; available from government agricultural organizations 

Local agronomists and botanists 

Entemologists may assist in insect species selection 


The allergens used for equine skin testing tend to be the same that is used for small 

animal testing, and often allergen selection has occurred with small animals in mind. 

Additional horse-specific allergens such as Culicoides are also included for the equine 

tests. Where horses are housed in the same metropolitan area, it is assumed that 

exposure to similar allergens as small animals will occur. However, modifications to 

the allergen selection may be necessary for horses from more distant country areas. 

It is not apparent whether particular allergens are relevant in horses, as their lifestyle 

may prevent significant exposure to various substances; such as insects (cockroach), 

House-dust mites and pollens from fodder materials brought into the area rather than 

grown in the area. Testing with epithelia (from other animals and humans) is not 

possible in Australia due to quarantine regulation against the importation of such 

allergens, so the significance of these is unknown in the Australian context. In one 

study in affected horses, positive intradermal test reactions to epithelia were seen in a 

significant number of clinically affected horses (54.2% to human dander!)(2). 

Allergen mixes are available, but testing with these is not recommended (1), as the 

concentration of the individual allergens in the mix becomes too dilute for detection. 

Variation in species of insect and pollen allergens may also be important. The 

Culicoides extract available through Greer laboratories is derived from Culicoides 

nebiculosis. In Australia, Culicoides brevitarsis is considered to be the only relevant species 

of Culicoides (at least in NSW, according to entomologists at the Elizabeth Macarthur 

Agricultural Institute - pers comm.). Information from Greer suggests that crossreactivity 

across most species of Culicoides can be expected, but the reality of this 

assumption is not known. 

20 


TABLE 1: CURRENT ALLERGENS SELECTED FOR INTRADERMAL 

TESTING BY VARIOUS CENTRES IN AUSTRALIA 

Melbourne Sydney Brisbane Perth 

Grass Pollens 

Bent 

Brome 

Canary (Phalaris) 

Cocksfoot 

Couch 

Couch, English 

Fescue 

Johnson grass 

Kentucky Bluegrass 

Maize 

Oat 

Orchard 

Paspalum 

Perennial Rye 

Prairie Grass 

Sweet Vernal 

Timothy 

Wheat, Cultivated 

Yorkshire Fog 

Weed Pollens 

 

Chenopodium mix 

Cocklebur 

Daisy 

Dandelion 

Dog Fennel) 

Fat Hen 

Lucerne (Alfalfa) 

Mexican Tea 

Mugwort 

Mustard 

Nettle 

Perennial Ragweed 

Plantain 

Ragweed, short 

Ragweed, Western 

Red Sorrel 

Rough Pigweed 

Sunflower 

Tobacco Leaf 


Tumbleweed 

Yellow 

Dock/Curled Dock 

Tree Pollens 

 

Alder 

Ash (Oregon) 

Birch (Birch mix) 

Birch, grey 

Casuarina 

Cypress 

Elm, cedar 

Elm, Chinese 

Eucalyptus 

Juniper 

Liquid Amber 

Maple 

Melaleuca 

Oak 

Oak, black 

Oak, red 

Oak, white 

Olive 

Palm 

Peppercorn (Pepper 

Tree) 

 

Pine (Pine mix) 

Pine, White 

Pine, yellow 

(Ponderosa) 

 

Plane Tree 

(Sycamore) 

 

Poplar 

Privet 

Wattle (Acacia spp) 

Willow, Arroyo 

Willow, black 

Moulds 

 

Alternaria 

Aspergillus 

Cladosporium 

Curvufaria 

Penicillium 

Insects 

 

Ant, Black 

22 


AmericanCockroach 

Cockroach mix 

Culicoides 

Deer Fly 

Flea 

Horse Fly 

House Fly 

Mosquito 

Moth 

Dust Mites 

 

D.farinae 

D.pteronyssinus 

Storage Mites 

 

Acarus siro (flour) 

Blomia tropicalis (grain) 

Lepidoglyphus destructor 

 

(fodder) 

Tyrophagus putrescentiae 

(cheese) 

 

Miscellaneous 

Carpet Grass Dialysate 

Carpet Grass 

Casuarina 1:40 

Casuarina Dialysate 1:40 

Grain Mill Dust Mix 

House Dust 

Kapok 

Kikuyu Dialysate 

Kikuyu Grass 

Kochia 

Malassezia 

Mixed feathers 

QLD Blue Couch 1:40 

QLD Blue Couch Dialysate 

1:40 

Allergen Dilution 

Red Clover 

Concentrations of allergens used for skin testing in horses in Australia have been 

based on those used for small animals, which were loosely derived from human 

studies and modified according to reactions in normal dogs in early work (10). In 

Australia, most allergens (grass, tree and weed pollens, moulds and insects) from 

Greer are tested at a concentration of 1000pnu (Protein Nitrogen Units), with some 

minor exceptions (15, 16). Dust mite and various other allergens are provided in 

weight per volume measurements (w/v), and the standard testing concentration for 

these is 1:10 000 which is roughly equivalent to 1000pnu. 


‘False positive’ results in equine intradermal tests are thought to be common (see 

further details under Interpretation of Results). To some extent, this may be a function of 

using extracts that are too concentrated and thus induce an ‘irritant’ reaction where 

true allergy is not present. 

Extensive work into determination of allergen threshold concentrations for 

intradermal testing in horses has not been undertaken. A recent study into insect 

allergens suggests that concentrations lower than 1000pnu may be more appropriate 

for horses (9), and offers some foundation for possible false positive reactions seen 

previously. The recommended testing concentration varied with the allergen, but for 

some allergens (particularly in the fly group) the concentration that evoked a positive 

response in 25% of normal horses was 250pnu/mL or less. 

Data is still being evaluated for a study the author has undertaken to determine 

pollen, insect, dust mite, mould and storage mite allergen threshold concentrations in 

normal horses. The aim of the study was to determine the concentration at which 

90% of normal horses would score (subjectively) less than 2 on the scale of 0 to 4 

commonly used by clinicians. The preliminary results suggest the following: 

24 

Many of the pollen concentrations may need to be increased (ie more 

concentrated) 

Results of the insect panel testing support the findings of Morris and 

Lindborg (9) that most concentrations need to be decreased from 1000pnu 

Dust mite concentrations may need to be dramatically decreased (ie more 

dilute) 

Mould concentrations may currently be somewhat too dilute 

The appropriate testing concentration of Culicoides appears to be around 1:10 

000 w/v, although the manufacturer recommends substantially more dilute 

concentrations than this (1:25 000 and 1:50 000) 

Storage mites commonly evoke strong delayed reactions, but in light of the 

immediate reading, higher concentrations than 1:10 000 may be more 

suitable 

It is apparent that the determination of threshold allergen concentrations is complex 

and there are many possible variables. It seems unlikely that a single testing 

concentration will be possible across the allergens for horses. The completed study 

will also assess any variations in relation to season and skin reactivity in normal 

horses. It is hoped that this data will greatly increase the reliability and accuracy of 

intradermal testing in horses. 

Solutions for skin testing should be made up fresh every 4 weeks, and stored in the 

refrigerator (and not allowing them to freeze repetitively) to maintain appropriate 

potency (16). 


Patient Preparation 

Drug Withdrawal 

Guidelines for drug withdrawal times in horses prior to skin testing are not based on 

scientific data, rather, they have been extrapolated from knowledge in small animals 

and with some degree of estimate. Recommended withdrawal times are as follows (1, 

16): 

Two to three weeks for inhaled, oral and topical corticosteroids (longer if 

oral corticosteroids have been given for extended periods) 

Eight weeks for injectable (‘depo’) corticosteroids 

Ten days for antihistamines 

Timing of skin testing 

There is conflicting evidence as to whether intradermal test reactivity declines with 

allergen season (17), but clinical experience tends to suggest that it does. Supposing 

that IgE remains adherent to mast cells in skin for a limited period (say 30 days), it 

appears sensible to test animals within 6 to 8 weeks of the end of their allergy season 

(1). Falsely negative results are commonly seen in seasonally allergic dogs tested out 

of their allergy season (18); it would be reasonable to suppose a similar situation exists 

in horses. Repeating the skin test during a different season may thus yield different 

results. 

Intradermal Testing Procedure 

1. Restraint for testing 

Sedation is recommended for skin testing all but the quietest horses, as a quicker and 

smoother injection process will ultimately mean less stress and better results to the 

animal. Several sedatives have been suggested for horse skin testing, again based on 

knowledge of drug interference in small animals. The Alpha 2 agonists are commonly 

used, registered sedatives in horses (19) that do not apparently interfere with skin 

testing in small animals (18). The author finds the sedation through Detomodine 

(Dormosedan; Pfizer) at a dose rate of 0.01 to 0.02 mg/kg IV (depending on the 

horses nature) both effective and suitable for skin testing. Reversal of sedation, 

although possible, is not generally carried out. 

The length of sedation achieved with this protocol is around 30 to 45 minutes, with a 

gradual increase in awareness from about 10 minutes into the sedation. 

Some horses, despite sedation, remain very reactive to the injection process and will 

toss their heads at every injection. A standard nose twitch is recommended for these 

horses. We have found that increasing the sedation for these horses appears to make 

no difference to this head tossing response; and where the test was repeated, applying 

the twitch and no sedation offered a similar level of restraint compared with the 


twitch and sedation previously. Caution should be given that not all horses tolerate a 

nose twitch well and common sense should prevail! 

2. Site Preparation 

The preferred site for skin testing is the lateral cervical neck above the jugular furrow, 

between the jaw and the shoulder. For a standard 80-injection skin test kit, an area 

around the size of an A4 sheet of paper is clipped with number 40 blades against the 

direction of hair growth. 

Where the skin is excessively dirty, gently cleaning with swabs moistened in plain 

water should provide a clean working surface. 

The author uses a template made of stiff plastic to ensure even spacing of the 

injection site ‘dots’. For 80 injections: 4 rows of 10 holes (about 2cm apart) were 

created in the template, and a waterproof white ‘paint-pen’ is used to mark the 

injection sites. Given that almost all horses have dark skin (even with a pale coat 

colour), a dark felt-tipped pen can be completely invisible, particularly when the skin 

test site is examined 24 hours after injection. 

3. Injection process 

Injections are administered intradermally above and below the injection markers. Using 

a 30-gauge needle and a 1ml syringe, approximately 0.05 to 0.1ml of solution is 

injected. The quantity injected appears to be based on personal preference of the 

clinician; provided the quantity is consistent for every injection in the test, there will 

be a relative correlation in the size of positive reactions. 

The first two and last two injections of every test should be the negative and positive 

controls of saline (or preferably allergen diluent) and histamine (1:100 000) 

respectively. The allergens are numbered at the base of the syringe plunger and 

injected in sequential numerical order. 

Some question remains as to whether needles need to be changed if the kit is to be 

used again for a different animal. This was discussed with equine veterinarians in 

Sydney who concluded it would be prudent to change needles between horses (and 

certainly between species of animals). Blood borne diseases that may be relevant in 

horses include: Equine morbillivirus (the zoonotic potential of this disease should 

also be observed), Equine infectious anaemia and viral arteritis. Even if the risk of 

these diseases is relatively low, the practitioners were keenly aware that veterinarians 

must be seen to be doing the ‘right thing’ in the eyes of their clients. 

4. Reading the injection sites 

It has been recommended that reactions be evaluated at 15 to 30 minutes after 

injection, and if possible at 45mins, 4 to 6 hours and at 24 to 48 hours (16). This may 

or may not be practical or relevant. 

26 


Each injection site is visually examined and gently palpated for changes in size, 

erythema and turgidity. Reactions are scaled subjectively as with small animals with a 

score of 0 (no increase in wheal size, using the negative control as a reference) to 4 

(large increase in wheal size, using the positive control as a reference), with 2 and 3 

reactions being somewhere in between. Reactions greater than 2/4 are considered to 

be positive (16). Some clinicians elect to also measure the wheal diameter to provide a 

more objective assessment of reactivity. 

Interpretation of Results 

What are we expecting to occur in an allergic individual? At a cellular level, relevant 

allergens will theoretically bind and bridge reaginic IgE antibodies on the surface of 

mast cells and result in mast cell degranulation resulting in wheal and flare reactions 

(16). 

It has been suggested that positive intradermal reactions be interpreted with caution 

in horses (1). Various studies have proposed that irritant reactions may be responsible 

for false positive results and allergen concentration in the test kit may need to be 

adjusted in horses as compared with small animals. In particular, allergens reported to 

evoke strong reactions in horses include Lucerne, grain mill dust, grain smuts, 

cottonseed, fireweed, yellowdock, Russian thistle, deer fly, Rhizopus spp., Candida 

albicans, black fly, horse fly, and black ant (1, 2, 5, 6, 7, 8). 

Several studies comparing reactions in normal horses and horses with a variety of 

allergic skin and respiratory diseases have concluded that normal horses will have one 

or more positive reactions, but that ‘allergic’ horses will have a significantly greater 

number of positive reactions; although the significance of reactions to individual 

allergens has been hard to interpret (1, 7, 8, 11, 12, 13, 14). 

Possible causes of false positive and false negative results are summarized in a table 2, 

extracted from Equine Dermatology by Scott and Miller (1). 


Table 2: Reasons for False Negative and False Positive Reactions in 

Intradermal Test Reactions 

Reasons for False Negative Reactions Reasons for False Positive Reactions 

Subcutaneous injections 

Too little allergen 

Testing with mixes 

Outdated allergens 

Allergens too dilute 

Too small volume of allergen 

injected 

Drug interference (Glucocorticoids, 

antihistamines, tranquilisers, 

progestational compounds, any 

drugs that lower blood pressure 

significantly) 

Anergy (testing during peak of 

hypersensitivity reaction) 

Inherent host factors (estrus, 

pregnancy, severe stress – systemic 

disease, fright, struggling) 

Off-season testing (1-2m after 

clinical signs have disappeared) 

Histamine ‘hyporeactivity’ 

28 

Irritant test allergens 

Allergen too concentrated 

Contaminated test allergens (bacteria, 

fungi) 

Skin-sensitising antibody only (prior 

clinical or present subclinical 

sensitivity – these reactions would be 

more appropriately termed clinically 

insignificant) 

Poor technique (trauma in needle 

placement, blunt needles, too large a 

volume injected, air injected) 

‘Irritable’ skin (large reactions seen to 

all injected substances, including 

saline control) 

Dermatographism 

Ectoparasitism (cross reactions with 

house dust mite extracts) 

Mitogenic allergen 

As further information about skin testing in horses comes to light, more accurate or 

reliable skin test results and useful assumptions about the results can be expected. At 

this stage, intradermal testing is still just one of the diagnostic modalities in the workup 

of allergy cases and the importance of other details in the case such as clinical 

signs, history, season of testing and other test results should not be overlooked. 


References 

1. Scott DW, Miller WH: Skin Immune System and Allergic Skin Disorders. In: 

Equine Dermatology. Saunders, Missouri, 2003 

2. Littlewood JD, Paterson S, Shaw SC. Atopy-Like Skin Disease in the Horse. 

In: Kwochka KW et al (eds). Advances in Veterinary Dermatology III. 

Butterworth-Heinemann, Boston, 1998 p 563 

3. Barbet JL et al: Diseases of the skin. In: Colahan PT et al (Eds). Equine 

Medicine and Surgery IV, Vol II. American Veterinary Publications, Inc, 

Goleta 1991, p 1569 

4. Byars DT: Allergic skin diseases in the horse. Vet Clin N Am Large Anim 

Pract 6: 87, 1984 

5. Rosenkrantz WS, Frank LA: Therapy of equine prusitus. In Ihrke RJ, et al 

(eds). Advances in Veterinary Dermatology II. Pergamon Press, Oxford, 1993, 

p433 

6. Fadok VA: Overview of Equine pruritus. Vet Clin N Am Equine Pract 11:1, 

1995 

7. Jose-Cunilleras E, Kohn CW, Hillier A, Saville WJA, Lorch, G: Intradermal 

testing in healthy horses and horses with chronic obstructive pulmonary 

disease, recurrent urticaria, or allergic dermatitis. J Am Vet Med Assoc 

219:1115, 2001 

8. Rosenkrantz WS et al: Responses in horses to intradermal challenge of insects 

and environmental allergens with specific immunotherapy. In: Kwochka KW, 

et al (Eds). Advances in Veterinary Dermatology III. Butterworth-Heinemann, 

Boston, 1998, p 200 

9. Morris DO, Lindborg, S: Determination of ‘irritant’ threshold concentrations 

for intradermal testing with allergenic extracts in normal horses. Veterinary 

Dermatology 14:31-36, 2003 

10. Willemse A, Van Den Brom WE: Evaluation of the intradermal allergy test in 

normal dogs. Research in Veterinary Science 32:57-61, 1982 

11. Fadok VA: Update on equine allergies. Vet Allergy Clin Immunology 5:68, 

1997 

12. Evans AG et al: Intradermal Testing of horses with chronic obstructive 

pulmonary disease and recurrent urticaria. Am J Vet Res 53:203, 1992 

13. Delger JM: Intradermal testing and immunotherapy in horses. Vet Med 92:635, 

1997 

14. Halliwell REW: The role of allergy in chronic pulmonary diseases of horses. J 

Am Vet Med Assoc 174:277, 1979 


15. Hensel P, Austel M, Medleau L, Zhao Y, Vidtashankar A: Determination of 

threshold concentrations of allergens and evaluation of two different histamine 

concentrations in canine intradermal testing. Vet Derm 15: 304-308, 2004 

16. Rosenkrantz W: Allergy Testing in Horses. Proceedings of the 5 th World 

Congress in Veterinary Dermatology, p244, 2004 

17. Nuttall T: Controversies in allergy testing. Proceedings of the 5 th World 

Congress in Veterinary Dermatology, p 367, 2004 

18. Scott, Miller, Griffin: Small Animal Dermatology, 6 th Edition. Eds: Muller and 

Kirk. WB Saunders, Pennsylvania 2001 

19. Freeman SL, England GC: Investigation of romifidine and detomodine for the 

clinical sedation of horses. The Veterinary Record 147: 507-511, 2000 

20. Fadok VA, Mullowney PC: Dermatologic diseases of horses, part 1. Parasitic 

dermatoses of the horse. Compend Cont Educ 5:S615, 1983 

21. Littlewood JD: Diagnostic procedures in equine skin disease. Equine Vet Educ 

9:174, 1997 

22. Mullowney PC: Dermatologic Diseases of horses part V: allergic, immunemediated 

and miscellaneous skin diseases. Compend continuing Educ 7:S217, 

1985 

23. Pascoe RR: The nature and treatment of skin conditions observed in horses in 

Queensland. Aust vet J 49:35, 1973 

24. Eder C, et al. Influence of environmental and genetic factors on allergenspecific 

immunoglobulin-E levels in sera from Lipizzan horses. Equine Vet J 

33:714 2001 

25. Quinn PJ, Baker KP, Morrow AN. Sweet itch: Responses of clinically normal 

and affected horses to intradermal challenge with extracts of biting insects. 

Equine Vet J 15:266-272 1983 

26. Kolm-Stark G, Wagner R: IDST in Icelandic horses in Austria. Equine Vet J 

34: 405, 2002 

27. Sloet van Oldruitenborgh-Oisterbann MM et al: Intradermal allergy testing in 

normal horses. In: Kwochka KW et al (eds). Advances in Veterinary 

Dermatology III. Butterworth-Heinemann, Boston, 1998 p 564 

28. Personal communication with Cathy McGowan from the University of 

Queensland 

30 


Intradermal Testing (IDT) in Horses: 

The UK Perspective 


Horses with a history of recurrent pruritus and /or urticaria represent the largest 

proportion of equine dermatology referral cases in the author's practice. Referred 

cases usually have a history of recurrent problems of at least 2 months duration. 

Ideally an elimination diet is undertaken before referral – although the almost 

complete absence of well-defined cases of adverse cutaneous food reaction in horses 

makes it a rare diagnosis, and so this is not considered essential, either prior to or 

after referral, although it is advised. Clients are often reluctant to limit their horses to 

strict, narrow elimination diets, particularly if they want to continue to work the 

horse. History and clinical examination are undertaken to rule out other possible 

causes of urticaria and pruritus, and if the signs are consistent with hypersensitivity, 

intradermal testing is undertaken. The author requests that horses be off 

antihistamines for a minimum of 2 weeks and have received no steroids for a month 

(ideally), although withdrawal of low dose alternate day steroids may not need to be 

for this period. Food additives, particularly aloe vera extract, should also be 

withdrawn – this advice is given on the basis of negative intradermal test results 

being obtained in a horse currently receiving aloe vera, with positive results obtained 

at retesting 3 weeks after withdrawal. 

Horses are sedated for intradermal testing, with detomidine hydrochloride (0.06- 

0.12mg/kg) and butorphanol 0.075-0.15mg/kg) intravenously. An area on the lateral 

aspect of the shoulder is clipped with a number 40 blade and injection sites marked 

with a permanent marker pen at 2 cm intervals. Allergens for testing are obtained 

from Greer Laboratories Inc., North Carolina, USA with additional forage mites 

supplied by Artuvetrin Biologicals nv, Lelystad, Netherlands. In the past allergens 

have also been supplied by Stallervet, France. The selection of allergens used in 

intradermal testing in dogs in the UK was originally based on advice obtained from 

colleagues in human allergy medicine and using information from publications and 

texts. Over the years the author has changed and refined the test kit, in conjunction 

with colleagues and in the light of frequency of negative and positive reactions. In 

fact, apart from the Culicoides antigen, which is restricted for testing of horses, the 

author currently uses the same allergens in dogs and horses. Allergens supplied from 

Greer are stored in concentrated form and diluted to testing strength, whereas the 

European allergens are supplied at testing strength. The testing strengths used are 

selected on the basis of advice from the allergen companies and from published data. 

The restrictions on experimentation in the UK mean that very little work has been 

done on optimising of allergen concentrations, apart from work done on Culicoides 


antigen concentration in the course of research projects conducted at the Royal 

Veterinary College, London. The author uses histamine at a concentration of 

2.75μg/ml as the positive control and phenolised normal saline as the negative 

control and an injection volume of 0.05ml. 

The allergens used in a study of 24 horses referred with recurrent or chronic pruritus 

and/or urticaria, but not typical of Culicoides hypersensitivity (Littlewood et al 1998), 

are listed in the following tables: 

TABLE 1 

Allergens used for intradermal skin testing obtained from Greer and 

Artuvetrin 

Allergen Concentration Allergen Concentration 

Ctenocephalides spp 1:1,000 w/v Weed pollens 

Tyrophagus putresceantiae 10 PNU/ml Mugwort 1,000 PNU/ml 

Acarus siro 10 PNU/ml Wild brassica 1,000 PNU/ml 

Dermatophagoides farinae 1:2,000 w/v Jerusalem oak 1,000 PNU/ml 

D. pteronyssinus 1:2,000 w/v Lamb’s quarter 1,000 PNU/ml 

Housedust 250 PNU/ml Daisy 1,000 PNU/ml 

Human dander 10 µg/ml Plantain 1,000 PNU/ml 

Cat dander 1,000 PNU/ml Sheep’s sorrel 1,000 PNU/ml 

Sheep epithelia 500 PNU/ml Yellow dock 1,000 PNU/ml 

Mixed feathers 1,000 PNU/ml Dandelion 1,000 PNU/ml 

Kapok 1,000 PNU/ml Clover 1,000 PNU/ml 

Tree pollens Nettle 1,000 PNU/ml 

Birch 1,000 PNU/ml Moulds 

Alder 1,000 PNU/ml Alternaria alternata 1,000 PNU/ml 

Hazel 1,000 PNU/ml Aspergillus fumigatus 1,000 PNU/ml 

Beech 1,000 PNU/ml Botrytis cinerae 1,000 PNU/ml 

Ash 1,000 PNU/ml Cladosporium herbarum 1,000 PNU/ml 

Sycamore 1,000 PNU/ml Epicoccum purpurascens 1,000 PNU/ml 

Poplar 1,000 PNU/ml Fusarium moniliforme 1,000 PNU/ml 

Oak 1,000 PNU/ml Helminthosporium sativum 1,000 PNU/ml 

Willow 1,000 PNU/ml Penicillium notatum 1,000 PNU/ml 

Grass pollens Phoma betae 1,000 PNU/ml 

Meadow grass 1,000 PNU/ml Pullularia pullulans 1,000 PNU/ml 

Fescue 1,000 PNU/ml Rhodotorula rubra 1,000 PNU/ml 

Cocksfoot 1,000 PNU/ml Cereal smuts 

Bent-grass 1,000 PNU/ml Barley smut 1,000 PNU/ml 

Italian rye grass 1,000 PNU/ml Oat smut 1,000 PNU/ml 

Timothy 1,000 PNU/ml Wheat smut 1,000 PNU/ml 

Key: PNU = protein nitrogen units; w/v = weight/volume dilution 

32 


TABLE 2 

Additional allergens used in a limited number number of horses, 

obtained mainly from Stallervet 

Allergen Concentration Allergen Concentration 

Euroglyphus maynei 1/1.000 w/v Grass pollens 

Dog dander * 1,000 PNU/ml Sweet vernal grass 10 IRU/ml 

Tree pollens Yorkshire fog 1/1,000 w/v 

Horse chestnut 1/1,000 w/v Perennial rye grass 10 IRU/ml 

Elm 1/1,000 w/v Couch grass 1/1,000 w/v 

Elder 1/1,000 w/v Weed/flower pollens 

Privet 1/1,000 w/v Ragweed 10 IRU/ml 

Lime 1/1,000 w/v Golden rod 1/1,000 w/v 

Moulds Wall pellitory 1/1,000 w/v 

Micropolysporum faeni + 100 µg/ml 

Key: w/v = weight/volume dilution; PNU = protein nitrogen units; IRU = immunoreactive units; 

• * = Greer allergen; + = Artuvetrin allergen 

TABLE 3 

Insect extracts used for equine intradermal skin testing, from Greer 

Allergen Concentration 

Mosquito (Culicidae) 1,000 PNU/ml 

Blackfly (Simulidae) 1,000 PNU/ml 

Horsefly (Tabanidae) 1,000 PNU/ml 

Culicoides spp 1/1,000 w/v 

1/10,000 w/v 

1/100,000 w/v 

Key: PNU = protein nitrogen units; w/v = weight volume dilution 

Horses were examined continuously for 30 minutes and the size of the positive and 

negative control wheals measured and recorded. Any wheals equal to or greater than 

the mean of the size of the control wheals were considered positive and diameters in 

millimetres recorded. Horses were examined again 4-6 hours later and note made of 

any positive reactions (criteria as before, using the histamine diameter at the 30minute 

time point). These reactions were considered immediate positive reactions. 

The owner or groom examined the test site 24-36 hours later and the presence of 

delayed reactions recorded and reported. 


The incidence of positive results in the series of cases was as follows: 

Allergen Positive 

reactions 

34 

Allergen Positive 

reactions 

Ctenocephalides spp 7/24 (2) Weed pollens 

Tyrophagus putresceantiae 13/23 (2) Mugwort 5/24 (1) 

Acarus siro 9/22 (2) Wild brassica 5/24 (1) 

Dermatophagoides farinae 18/24 (4) Jerusalem oak 4/21 

D. pteronyssinus 19/24 (3) Lamb’s quarter 3/24 

Housedust 17/21 (2) Daisy 8/24 

Human dander 13/24 (2) Plantain 3/24 

Cat dander 3/24 (1) Sheep’s sorrel 2/24 (1) 

Sheep epithelia 8/24 Yellow dock 4 (1) 

Mixed feathers 9/24 (2) Dandelion 4/24 (2) 

Kapok 2/21 (1) Clover 8/21 

Tree pollens Nettle 6/24 

Birch 2/24 (1) Moulds 

Alder 2/24 (1) Alternaria alternata 2/24 (1) 

Hazel 3/24 (1) Aspergillus fumigatus 3/23 (1) 

Beech 3/24 (1) Botrytis cinerae 4/20 (1) 

Ash 2/24 (1) Cladosporium herbarum 5/23 (1) 

Sycamore 2/21 (1) Epicoccum purpurascens 5/20 

Poplar 5/24 (1) Fusarium moniliforme 4/20 

Oak 3/24 (1) Helminthosporium sativum 3/20 

Willow 3/24 Penicillium notatum 2/23 

Grass pollens Phoma betae 3/20 

Meadow grass 2/24 Pullularia pullulans 4/19 (1) 

Fescue 2/24 Rhodotorula rubra 2/20 (2) 

Cocksfoot 3/24 (1) Cereal smuts 

Bent-grass 2/24 (1) Barley smut 10/24 (2) 

Italian rye grass 4/21 (1) Oat smut 10/24 (2) 

Timothy 2/24 (1) Wheat smut 8/23 (2) 

Allergen Positive Allergen Positive 

reactions 

reactions 

Euroglyphus maynei 1/3 Grass pollens 

Dog dander * 2/3 Sweet vernal grass 0/3 

Tree pollens Yorkshire fog 0/3 

Horse chestnut 0/3 Perennial rye grass 0/3 

Elm 1/3 Couch grass 1/3 

Elder 1/3 Weed/flower pollens 

Privet 1/3 Ragweed 0/3 

Lime 1/3 Golden rod 0/3 

Moulds Wall pellitory 0/3 

Micropolysporum faeni+ 1/2 


Allergen Positive reactions 

Mosquito (Culicidae) 2/11 

Blackfly (Simulidae) 3/11 

Horsefly (Tabanidae) 2/11 

Culicoides spp 6/13 

10-fold dilution 6/13 (1) 

100-fold dilution 4/13 

Delayed reactions in parentheses and underlined 

All horses showed at least two immediate positive reactions; in some cases reactions 

were not evident until the 4-hour time point. Twelve horses showed delayed 

(>24hour) reactions, not necessarily preceded by immediate or late-immediate 

reactions. Two horses reacted to all allergens tested; in both cases the negative 

control did not produce a wheal reaction, nor did application of mechanical pressure, 

ruling out dermatographism as the cause of the multiple reactions. Reactions to mite 

extracts were common; only 2 horses (8.3%) showed no reactions to any mite 

species. Dust mite reactions were seen in 20/24 (83.3%); 58.3% reacted to both dust 

and forage mites, 25% to dust mites alone. Two horses reacted to forage mites but 

not dust mites. Housedust reactions were also common, occurring in 81% of cases. 

Reactions to epithelial extracts were also frequent; 54.2% reacted to human dander, 

33.3% to sheep and 12.5% to cats; in all of the latter cases there were yard cats that 

had access to the stables and tack rooms and often slept on rugs or in the stables. 

Feather reactions were also quite common (37.5%), including two delayed reactions; 

two cases improved dramatically following removal of birds nests and preventing 

further access of birds, with complete resolution of skin disease without any other 

interventions. 

The majority of cases showed reactions to pollens; 10/24 (41.7%) did not. Weed 

pollen reactions were the most common - seen in 13 horses (54.2%), with nine 

(37.5%) having reactions to tree pollens and five (20.8%) to grasses. In a number of 

cases the history suggested that exposure to grass and weed pollens in meadow hay 

were relevant. A few positive reactions to each of the moulds were noted. A 

considerable number of cases showed reactions to cereal smuts – 41.7% to barley 

smut, 41.7% to oat smut and 34.8% to wheat smut. 

Six horses developed immediate and delayed reactions to biting insects, particularly 

Culicoides. Horses with reactions to mosquito, blackfly and horsefly extracts were also 

positive to Culicoides. All of these cases had a history of clinical signs consistent with 

“sweet itch”, but all showed additional symptoms that were not typical of summer 

recurrent seasonal hypersensitivity. Together with two further cases that had 

consistent history and clinical signs but were not tested with insect extracts, these 

horses were considered to be suffering from both atopic dermatitis and insect bite 

hypersensitivity (33.3% of cases). 

Reference: 

Littlewood JD, Paterson S, & Shaw SC. (1998) Atopy-like skin disease in the horse. Advances 

in Veterinary Dermatology 3, p563 


36 

Contact Atopy in Five Horses on the 

Same Property 

History and Presentation 


Ken Mason 

Five of 20 horses on a single property had developed a pruritic dermatitis over 

several years. The affected horses were approximately 10 to 15 years old having been 

obtained as adults. The five were a grey Arab cross gelding, a bay thoroughbred 

gelding a grey Dartmoor cross pony mare and a mare and a gelding Percherons. 

The history indicated that the skin problem started in summer and progressed 

through till autumn then settled in winter to spring. 

Examination results 

All horses were in good condition and seemed well systemically. The clinical signs 

were of a very itchy dermatitis on the limbs and face only and seemed to show a 

water line effect below which primary lesions were erythema and macular papular 

eruptions and secondary lesions of self trauma causing exudative and bleeding 

abrasions and alopecia. 

Test results 

Intradermal skin testing with a panel of environmental allergens including typical 

insects found around horses on the grey Arab cross gelding revealed several grass 

and insect positive reactions. Scratch testing with parts of plants collected from the 

paddocks in which the horses grazed revealed positive immediate reactions to the 

pasture grasses kikuyu (Pennisetum clandestinum)and couch (Cynodon spp.) and billy goat 

weed (Ageratum houstonianum) but no reaction to sow grass (Paspalum conjugatum bergius) 

and broad leaf paspalum (Paspalum dilatum). Isolation of the horses into dirt floored 

yards( with no plants) adjacent to the grazing paddocks resulted in all skin signs 

disappearing. Returning the horses to the grazing paddocks caused return of the skin 

lesions. 

Discussion 

The grey Arab horse tested and reactive on test to kikuyu, couch and billy goat weed 

had lesions that corresponded to the height of these plants touching the limbs and 

face when the horse was feeding. One throughbreed not allergy tested had lesions

much higher and corresponded to the much taller sow grass. The owner reported 

that the horse refused to pass through patched of this grass when it was "seeding" 

and if forced to would stomp its feet and chew at the limbs where the grass had 

touched the skin. Washing the limbs down and isolating the horse off the paddock 

with this grass and broad leaf paspalum resulted in signs resolving. 

Thus it would seem that these horses had contact allergy to these pasture plants and 

that the other insect reactions and pollens to which it was positive on intradermal 

skin test were not related to the skin lesions, as the horses would have still been 

exposed to these environmental allergens while yarded adjacent to the grazing 

paddocks. The paddock plants suspected to be the cause due to positive allergy 

tested with a crude saline extract were only allergic when pollen and seed heads were 

developed in summer and autumn. 


38 

Immunotherapy for Equine Atopic 

Dermatitis 



Allergen-specific immunotherapy (ASIT) is widely used in small animal dermatology 

in the management of atopic dermatitis and in some countries for atopic humans. 

ASIT is indicated in in animals in which avoidance of allergens is not possible or is 

ineffective, where signs are pesent for more than 4-6 months of the year, and drugs 

for symptomatic control are ineffective, or required at excessively high doses, or are 

contraindicated (Scott & Miller 2003). Since the author has had very few cases that 

fall into the above category, she has only limited personal experience with 

immunotherapy in the horse and this presentation will draw on published 

information. 

The mechanisms of action of immunotherapy are complex and the details of their 

action still poorly characterised. Various hypotheses put forward historically include 

humoral desensitisation (reduced IgE production), immunisation (blocking IgG 

antibodies), cellular desensitisation (reduced reactivity of mast cells and basophils, 

induction of tolerance (generation of allergen-specific suppressor cells) and 

combinations of the above. However, in patients with good clinical responses to 

immunotherapy vaccine, there may be no decrease and even increases in IgE 

concentrations. Increased numbers of CD25+ T-suppressor lymphocytes has been 

shown to correlate with a favourable response, indicating that the major beneficial 

effect is cellular rather than humoral. 

There is a scarcity of published studies demonstrating the efficacy of ASIT in horses 

in prospective, randomised, controlled trials, although a number of publications 

report the clinical benefits in retrospective case studies. Overall success rates that are 

reported are remarkably similar to those reported for ASIT in dogs and cats, with 

60-71% of cases having a good to excellent response, when therapy is based on 

intradermal testing. Most published reports have used aqueous allergens, with a 

variety of protocols used. Although there are some theoretical objections raised to 

the use of alum-precipitated vaccines (potential to further stimulate Th 2 type of 

response and enhanced IgE production) experience with small animals would 

suggest that these are not clinically relevant, with the only randomised, blinded, 

placebo-controlled trial of ASIT in atopic dogs using an alum-precipitated vaccine,

and this and other uncontrolled trials using alum-precipitated vaccine having very 

similar rates of success compared with aqueous vaccines (~60-70% of cases showing 

good to excellent/greater than 50% improvement). 

There is controversy regarding the benefits of ASIT using insect extracts. A 

randomised, double-blinded, placebo-controlled clinical trial of ASIT for Culicoides 

hypersensitive horses involving 14 horses over a 6-month period demonstrated no 

difference between verum and placebo treated groups (Barbet 1990). However, a 

later Canadian open study conducted over 1-2 years with a crude Culicoides extract 

injected into 10 horses severely affected by disease resulted in a reduction of clinical 

signs in 9/10 (90%) in the first year. Of the eight horses treated during the second 

year, three were free of clinical signs at the end of the year(37.5%), three showed 

much less severe signs(37.5%), and two (25%) showed moderate reduction in clinical 

signs (Anderson et al 1996). 

In a retrospective study of 43 horses with allergic skin disease, of which 33 had been 

on immunotherapy for a minimum of 4 months the following data were reported 

(Rosenkrantz 1992): 10 horses showed pruritus only, 14 were urticarial and 9 had 

pruritus and urticaria. Good-to-excellent responses to ASIT were reported in 60% of 

the pruritic horses, 71% of the urticaria cases and 66% of the horses with both 

urticaria and pruritus. Another study (Fadok 1996) showed that in horses that were 

purely atopic 5/7 (71.4%) were greater than 50% improved and 7/13 (53.8%) 

atopic and insect-allergic horses were greater than 50% improved, whereas 3 of 4 

(75%) insect-only allergic horses had no response to immunotherapy. 

A subsequent study of symptomatic horses with positive intradermal responses to 

insect and environmental allergens evaluated the efficacy of insect hyposensitisation 

compared to insect and environmental hyposensitisation in a double-blinded, 

placebo-controlled study (Rosenkrantz et al 1998). Clinical scores were ascribed for 

pruritus, excoriations, scale-crust and alopecia) ranging from 1-10 for affected 

regions of the body and mean scores ascribed. Cases were re-evaluated after 3 

months and those that had received placebo were allowed to receive verum 

treatment, and subsequently horses in the insect-only treatment group were 

permitted to convert to insect + environmental ASIT. Analysis of clinical scores 

after the initial 3 months treatment showed no statistically significant difference 

between the placebo and verum treated groups with either formulation of 

immunotherapy. However, when the pre-treatment and post-treatment scores for 

individual horses were analysed, there was a significant difference in verum treated 

animals compared to the placebo groups. Similarly, when the placebo groups were 

changed to verum treatments, statistically significant changes in scores were 

achieved. There was no significance in changing from insect only to insect + 

environmental ASIT. Minor reactions characterised by swelling at the injection site 

was observed in six of 27 horses receiving ASIT, but all reactions subsided in 24-72 

hours. 


Recommendations: 

Allergens should be selected on the basis of positive intradermal test responses, 

incorporating all those that appear to be relevant in view of the history and 

environmental exposure. In multiply allergic horses, more detailed information may 

be needed regarding likely presence of allergens in that individual's environment, the 

allergens know to be important in that geographical region, and the duration of the 

presence of the allergen. Cross-reactivity within groups of allergens may be utilised 

in making selections; cross-reactivity is likely in plants of the same genus and family. 

In general grasses are the most cross-reactive and weeds less so. Mould and 

arthropod allergens contain proteases that may have adverse effects on other 

allergens when used in combination, which may or may not affect the success of 

hyposensitisation. 

Beneficial effects may be seen as early as 2-3 months into treatment, but may take as 

long as a year to achieve benefit. Intervals between maintenance injections can be 

tailored to the individual, according to the reappearance of clinical signs, varying 

between weekly to monthly. Frequency of injections may very at different times of 

the year. In general, lifelong administration of vaccine is required. Adverse reactions 

are uncommon and usually mild. Reactions may include intensification of clinical 

signs for a few hours to a few days after injection, local injection site reactions 

(swelling +/- pain) and urticaria. Serious, anaphylactic reactions are extremely rare. 

Reactions are treated symptomatically. Exacerbation of clinical signs is an indication 

to reduce to dose of vaccine. Severely affected horses may need additional 

glucocorticoid therapy to control their symptoms, but low-dose alternate day 

prednisolone can be used in conjunction with ASIT, just as in small animal patients, 

and immunotherapy still be successful at controlling the disease, with lower doses of 

steroids than were required before or even subsequent withdrawal of steroids. 

References: 

Anderson GS, Belton P, Jahren E, Lange H & Kleider N (1996) Immunotherapy 

trial for horses in British Columbia with Culicoides (Diptera: Ceratopogonidae) 

hypersensitivity. Journal of Medical Entomology 33, 458-66 

Barbet JL, Bevier D & Greiner EC. (1990) Specific immunotherapy in the treatment 

of Culicoides hypersensitive horses: a double blind study. Equine Veterinary Journal 22, 

232-5 

Fadok VA (1996) Hyposensitisation of Equids with allergic skin/pulmonary disease. 

Proceedings of the Annual Meeting of the American Academy and College of Veterinary 

Dermatology , Las Vegas, Nevada p47 

Rees CA (2001) Response to immunotherapy in six related horses with urticaria 

secondary to atopy. Journal of the American Veterinary Medical Association 218, 753-5 

Rosenkrantz WS (1992) Therapy of equine pruritus. Proceedings of the 2 nd World Congress 

of Veterinary Dermatology Montreal, Canada p 435 

40 


Introduction 

Diagnostic Approach to Urticaria 

Reg Pascoe 

Horses show the greatest incidence of urticaria of all the species of domestic animals. 

Urticaria is a specific skin lesion rather than a specific disease entity. It has many 

different aetiologies and pathogenesis (Logas & Barbet 1999). Generally, it is discussed 

as a single entity even though its clinical manifestations vary from a minor transitory 

nature to major systemic life endangering problems. 

Aetiology / Pathophysiology 

The pathogenesis of equine urticaria is not well understood. Urticaria has been 

associated with immunological and nonimmunological mechanisms leading to the 

release of various mediators by mast cells. In a study by Rufnacht et al (2004) skin 

biopsies of 32 horses with a history of urticaria were stained with toluidine blue, a 

double-labelling method for chymase and tryptase, plus immunohistochemistry for 

immunoglobulin IgE. These horses were compared with horses with pemphigus 

foliaceus, insect bite hypersensitivity and control horses with healthy skin. Neither 

formalin fixation time nor biopsy site influenced the staining methods.No chymasepositive 

cells were found. In all groups of horses, cells staining with toluidine blue and 

for tryptase and IgE were found in the epidermis and hair follicle papilla and 

significantly more positively staining cells were observed in the subepidermal dermis 

compared with the deep dermis. Horses with urticaria had significantly more IgEbearing 

cells in the subepidermal dermis than control horses. However, horses with 

urticaria had significantly fewer toluidine-blue-stained mast cells in both subepidermal 

and deep dermis compared with the insect bite hypersensitivity and pemphigus 

foliaceus groups. 

This study supports IgE-mediated reactions play a role in the pathogenesis of urticaria. 

The use of intradermal testing (IDT) of urticaria and atopy also can be equivocal as 

Evans et al (1992) had found that positive results were also obtained from horses not 

showing signs of atopy. Further studies (Lorch et al 2001) have assisted in the 

elucidation of more of the quandary associated with IDT 

Many causes of urticaria have been suggested. (Scott & Miller 2003) 

1. Degranulation of mast cells and basophils is presumed to be the basic 

pathogenesis. Liberation of chemical mediators, which cause increased vascular 

permeability leads to wheal formation. 


42 

2. Immunological: hypersensitivity where antigen/allergen probably reaches the 

skin via the systemic route rather than by local contact. The antigen reaches the 

systemic circulation mechanisms involved include type 1 and 111 

hypersensivity reactions 

• Injection (drugs such as some antibiotics, BTZ, Ivermectin, Moxidexin, 

pethidine, Vit B complex, flunixen, iron dextran and many others) 

• Ingestion (chemical, feeds pasture plants) 

• Inhalation (pollen, dust, chemicals, moulds) 

• Vaccines (strangles, botulism, salmonella, tetanus etc) 

• Transfusion reactions 

• Biting insects (biting flies, mosquitoes, blackflies,bees, wasps, spiders etc) 

• Infections (bacterial, fungal, viral parasites such as onchocerciasis, habronemiasis,) 

• Vasculitis (streps, purpura haemorrhagica) 

3. Allergic urticaria: 

• Atopy 

• Drug related 

• Food allergy 

• Inhaled antigens, pollens, moulds 

• Contact allergy (very rare); must be carefully distinguished from allergic contact 

dermatitis. 

4. Physical urticaria, non-immunological pathogenesis. 

• Dermatographism: wheal developing from blunt scratch on skin 

• Cold urticaria, heat and light 

• Exercise induced urticaria 

Clinical Presentation 

There is no breed, age or sex predilection. Onset can be peracute to acute with signs 

developing within minutes up to a few hours and usually resolve in 24-48 hours 

occasional signs can last up to 6-8 weeks. Or in the instance of recurrent urticaria it 

may be chronic or persistent if present for more than 8 weeks 

Lesions 

An oedematous lesion of the skin or mucous membrane is called a wheal, which is a 

flat topped papule/nodule with steep walled sides which pits on pressure. Some have 

slightly depressed centres. 


Wheals vary in size and shape and quite arbitrarily may be divided into: 

1. Conventional: 2-3mm up to 3-5mm. 

2. Papular: multiple small uniform 3-6mm diameter wheals i.e. insect bites. 

3. Giant: either single or coalesced multiple wheals up to 20-30cm diameter. 

4. Annular: donut like lesions. 

The lesion may present differently depending on the location of the oedema i.e. 

whether it is in the upper layers of the dermis or subcutaneous and may be pruritic or 

non pruritic. 

1. "Oozing urticaria" - where dermal oedema is severe, oozing of serum from 

the skin surface may occur. Care should be taken to distinguish this from an 

erosive/ulcerative process or a pyoderma. NB lesion must still pit on pressure. 

2. Gyrate urticaria - has been referred to as the dermal form of erythema 

multiforme but it should be stressed that this syndrome is not related to 'true' 

erythema multiforme which is primarily an epidermal disease (lesions DO NOT 

pit on pressure). Drug reactions appear to be the most common cause of this 

form of urticaria. 

3. Angiooedema (Angioneurotic oedema) - a subcutaneous form of urticaria 

which tends to be more diffuse due to lack of restraint to spread in the sub 

cutis. Usually involves the head and extremities and is more indicative of a 

systemic and serious disease than urticaria. 

Diagnosis 

Because of the numerous potential causes of urticaria a definitive diagnosis may only be 

reached after extensive clinical and diagnostic investigation which can be time 

consuming, expensive and often unrewarding. Horse owners usually are reluctant to 

undertake the costly task of endeavouring to obtain an accurate diagnosis. 

Initially, diagnosis is mostly based on clinical signs (mostly cutaneous reaction patterns) 

and a careful history of the case. (Scott & Miller 2003) 

History is important: 

- Is it the first attack? 

- If not, how many and are they seasonal? 

- Site of lesions- is it a point of contact with gear? 

- Use of any drugs, frequency and reaction at time of use, drenches, 

medicated sprays, ointments, shampoos, ultrasound gel. Etc 

- Pasture plants 

Specific activities-exercise only induced 

Being worked, (confirm by 30 min exercise producing urticaria) out 

in paddock for pick of grass 

- Food allergy can only be traced by elimination diets and then 

challenge with suspected feed ( very time consuming with NO short 


44 

cuts) 

- Heat: over rugging to cause higher than normal body heat and poor 

loss of retained heat e.g. Show horses over rugged to induce hair 

changes 

- Cold: ‘Cold' urticaria: use ice cube - oedema in 15 minutes 

- Pressure induced-dermatographism by coarse instrument: scratch, 

wheals appear in

References 

Evans AG, Paradis MR & O’Callaghan M (1992) Intradermal testing of horses with 

chronic obstructive pulmonary disease and recurrent urticaria. 

American Journal of Veterinary Research 53: 203–8. 

Logas DB & Barbet JL (1999) Inflammatory, infectious and immune disease. In: 

Colahan PT, Merritt AM, Moore JN eds. Equine Medicine and Surgery. St. Louis, 

MO: Mosby Year Book 1999, 1868–73. 

Lorch G, Hillier A, Kwochka KW. Saville WA & Le Roy BE (2001) Results of 

intradermal tests in horses without atopy and horses with atopic dermatitis or 

recurrent urticaria. American Journal of Veterinary Research; 62: 1051–9. 

Rüfenacht S, Marti E, Von Tscharner C, Doherr MG, Forster U, Welle M & Roosje 

PJ (2005) Immunoglobulin E-bearing cells and mast cells in skin biopsies of horses 

with urticaria Veterinary Dermatology 16, 94–101 

Scott DW & Miller WH (2003) Equine Dermatology Elsevier Science (USA) 

Philadelphia PA .USA 


Erythema multiforme 

Rare, acute, self-limiting, urticarial, maculopapular or vesico-bullous dermatosis. Other 

triggering influences such as drugs, infections (especially Herpes virus), and tumours - 

especially lymphoreticular neoplasms. Many cases are classified as idiopathic. 


Can be considered a type of allergic response, being very similar to graft versus host 

reaction. 

Clinical presentation 

Lesions tend to have a symmetrical distribution. Asymptomatic cutaneous eruptions. 

Characteristic 'donut like' skin urticarial lesions develop rapidly from initial urticaria and 

plaques. Occasionally involves mucous membranes of mouth. Persist from days to 

weeks. No scaling, crusting or alopecia in many horses. These plaques do not pit on 

pressure 

Differential diagnosis 

Urticaria, amyloidosis, mastocytoma, lymphosarcoma, fixed drug reaction, toxic 

epidermal necrolysis. 

Diagnosis 

Skin biopsy. 

Management 

Runs benign course over 2-3 months. Recurrence reported in some cases. 

Prognosis 

Guarded to poor for permanent recovery. 

46 


Introduction: 

Equine Chronic Urticaria 

Greg Burton 

Urticaria (hives) are relatively common in horses. Chronic urticaria is an ill-defined 

syndrome in the horse whereby transient urticarial eruptions occur in a recurrent 

fashion over a period of greater than 6 to 8 weeks. Chronic urticaria in people is 

more clearly defined as urticarial eruptions that occur at least twice weekly for greater 

than 6 weeks. 

Pathogenesis: 

The pathogenesis is poorly understood. Both immunological and nonimmunological 

mechanisms are considered likely. The major effector cell is likely to 

be the mast cell however basophils, mononuclear cells, platelets and endothelial cells 

may also play a role. Increased IgE bearing cells have been identified in skin 

biopsies of horses with urticaria. 

Potential triggers 

- type 1 and type III hypersensitivity reactions (atopy, adverse food 

reactions, contact reactions, arthropod bites, parasites) 

- physical triggers (sunlight, pressure, heat, cold and exercise) 

- psychological stress 

- drugs (ivermectin, various antibiotics, NSAIDs) 

- idiopathy 


There is no reported age, breed or sex predisposition in horses with urticaria. 

Urticarial lesions appear suddenly, are often generalised and somewhat symmetrical, 

are associated with variable pruritus and usually not associated with oozing of serum 

or haemorrhage. They are variable sized from a few millimetres to several 

centimetres with sharply demarcated edges and flat tops. The lesions are not painful, 

have normal body temperature and pit on pressure. They are effervescent and 

resolve within 24 hours. A clinical classification exists and may have some 

aetiological significance. 

I. Conventional urticaria: papules and wheals of 2-5mm diameter 

II. Papular urticaria: uniform 3-6mm papules and often associated with 

insect bites, especially mosquitoes 

III. Giant urticaria: up to 40cm diameter 


48 

IV. Exudative urticaria: associated with serum oozing and matting of the 

hair and hair loss. 

V. Gyrate urticaria: bizarre serpiginous and arciform shapes and often 

associated with drug reactions. 

Differential diagnoses: 

- folliculitides 

- vasculitis 

- erythema multiforme 

- cutaneous infiltrates (amyloidosis, neoplasia) 

- 

Diagnosis: 

History 

- record of client observations (seasonality, drug exposure, feeds, housing, 

environment, association with exercise) 

- Duration of the lesions 

- Location of the lesions (contact sites?) 

- Grooming protocol 

- Parasite control 

A thorough history should allow you to rule in/out drugs, parasitism, infections and 

give clues as to the likelihood of physical urticaria. 

Diagnostic tests 

Treatment: 

- Permanent marking pen to assess persistence of individual lesions 

- Histopathology for lesions that persist greater than 24 hours (infiltrative 

urticaria, vasculitis) 

- Assess for dermatographism (blunt pressure applied and observe for 

wheal formation) 

- Local application of heat (water > 44 o C) or cold (ice cube) 

- Exercise challenge 

- IDT (intradermal skin testing for airborne allergens) 

- Hymenoptera testing 

- Novel protein hypoallergenic diet 6 to 8 weeks 

- Avoidance of triggers if identified 

- Trigger “desensitisation” 


Acute treatment 

- Epinephrine 1:1000, 5 to 10 mls/450kg IM (given acutely) 

- Prednisolone 2mg/kg (given acutely) 

Chronic treatment 

Conclusion: 

- ASIT (allergen specific immunotherapy) 

- Antihistamines (hydroxyzine 400-500mg bid +/-cyproheptadine 20mg 

bid) 

Most common cause, once drugs are ruled out, is atopic dermatitis. Further 

elucidation of ideal concentration of allergens for IDT in the horse would lead to 

greater utilisation of IDT as a diagnostic step and ASIT as a therapeutic option for 

chronic urticaria in the horse. 

. 


50 

Management of the Atopic Horse 



Once a diagnosis of atopic dermatitis has been made in any companion animal, the 

various therapeutic options available need to be considered and discussed with the 

client. As with any hypersensitivity condition, allergen avoidance is the ideal solution, 

but this may not be achievable, depending on the trigger factors implicated. Other 

therapeutic approaches include hyposensitisation (immunotherapy), other 

immunomodulatory approaches and symptomatic ant-inflammatory and anti-pruritic 

treatments. 

Allergen avoidance: 

For horses with clinical disease related to indoor allergens, maintaining the horse at 

pasture all the year round is the ideal solution. However, for horses with pollen 

allergies and insect bite hypersensitivity, keeping the horse stabled for the majority of 

the time is more appropriate. Treatment of horses with insect bite hypersensitivity 

will be covered in a later presentation and will not be addressed further in this 

presentation. Those patients with both indoor and outdoor allergens implicated in 

their disease process are the most challenging in terms of allergen avoidance. 

Nonetheless, it is possible with management modification to reduce allergen 

exposure in the indoor environment, which, in the author's experience, can be very 

effective in controlling the disease in many patients. 

Management measures that are recommended include housing the horse in a stable 

with its own air space, but with good ventilation, not underneath or next to a 

hay/grain loft or store, removal of birds nests, removal of all loose bedding, 

vacuuming and pressure cleaning of the stable interior on a regular basis. Rubber 

matting is the ideal flooring, with no loose bedding at all, since even “low allergen”, 

dust-free beddings may provide a suitable micro-environment for dust and storage 

mite species. This flooring is well tolerated by even the largest horses, although 

owners tend to anthropomorphise about the comfort of their horse! 

Feeding of low allergen foods may also be helpful – such as vacuum-packed wilted 

grass products, or blow-dried (dust-free) ley-grown hay, and cubed rather than loose 

grain concentrate foods. 

For horses with reactions to dust mite species that show lesions on the skin under 

rugs, presumably due to mites living in the rugs/horse duvets, the author has had

anecdotal success with use of human dust mite-proof bedding covers, for example 

using a dust mite-proof mattress cover or duvet cover next to the horse's skin, 

underneath the other rugs. This has been beneficial in cases that persisted with 

lesions in spite of regular laundering of rugs. 

Immunotherapy: 

Immunotherapy is indicated for horses that are not adequately controlled by allergen 

avoidance measures and for those that have pollen reactions, unless they are to 

plants with a very narrow pollination season, where symptomatic treatment may be 

more appropriate. Allergen selection for formulation of vaccine requires making 

judgements about which positive intradermal reactions are clinically significant and 

whether or not to include insect extracts in a vaccine. The author's practice is to 

recommend allergen avoidance measures in the first instance – both environmental 

and insect control – and to consider immunotherapy in those patients where there is 

still significant ongoing clinical disease. 

Immunomodulatory approaches other than allergen-specific are under active 

development, utilising naturally occurring, bacterial-derived, immunomodulators to 

down-regulate T-helper 2 and optimise T-helper 1 mechanisms. Extracts under 

investigation contain immunomodulators that occur in the bacterial cell wall, 

bacterial heat-shock proteins that share homology with mammalian mitochondrialderived 

stress proteins and bacterial sugars related to innate immunity and to the 

bacteriomimetic sugars presented on the surfaces of rapidly replicating mammalian 

cells, such as those of neoplasms and inflammatory responses. 

There is in the UK a clinical trial underway, under a VMD test certificate, of a 

bacterial-derived product in horses with a clinical diagnosis of 

Culicoides hypersensitivity. Two hundred susceptible horses are recruited to the trial, 

which is running over this year and into next year, with both open and randomised 

elements to the trial. No data will be available until later this year, but in a small 

placebo-controlled pilot trial the product has been demonstrated to statistically 

significantly reduce the severity of disease. Future results are awaited with interest. 

Glucocorticoids: 

Severely affected horses, particularly those with marked pruritus and those with 

chronic changes related to insect bite hypersensitivity, may well need systemic steroid 

therapy. There are often concerns about the risks of steroid therapy in horses, but at 

the anti-inflammatory dose rates required for allergic patients the risks are 

considered very low, unless there is a history of laminitis. 

Prednisolone is the author's drug of choice, given orally at an initial dose rate of 0.5- 

1mg/kg/day. Daily therapy used continued until the clinical signs are controlled, 

usually within 1-2 weeks, then reduced to alternate day therapy, with gradual tapering 

of the dose to the lowest possible maintenance dose as long as is needed. This 


usually ends up in the range of 0.2-0.5mg/kg every other day. The author has had no 

problems dropping from the initial once daily dose to the same dose on alternate 

days for atopic horses (in contrast to patients with immune mediated disease). Some 

clinicians prefer to use an initial parenteral dose of dexamethasone – 0.02-0.1mg/kg; 

oral dexamethasone can be administered thereafter, in the dose range of 0.01- 

0.02mg/kg every 2-3 days. 

In addition to laminitis, the other side effect concerns would be potentiation of 

existing infections or increased susceptibility to infection, particularly opportunistic 

respiratory infections. At the doses required for management of most allergic horses, 

this does not present a big problem in the experience of the author. 

Antihistamines: 

Drugs that block the cellular receptors for histamine may be utilised in allergic 

horses. In the UK there are no veterinary licensed antihistamines, but human 

products are used off-label. The drug used most commonly by equine practitioners is 

hydroxyzine hydrochloride; doses of 0.5 -1.5mg/kg every 8-12 hours are suggested 

in the literature. Others that may be used in the horse are chlorpheniramine 

0.25mg/kg every 12 hours and diphenhydramine 0.75-1mg/kg every 12 hours. 

Doxepin hydrochloride is a tricyclic antidepressant with H1-receptor blocking 

effects and has been reported to be useful in some pruritic horses at dose rates of 

0.5-0.75mg/kg every 12 hours. 

Antihistamines may be more effective for cases of urticaria than pruritus. Although 

the systemic side effects of antihistamines may be of less concern than for steroids, 

sedation and personality changes may occur and these drugs are not permitted in 

horses competing under certain regulatory authorities. Recommended withdrawal 

times should be checked with the relevant bodies for competition horses. 

Essential Fatty Acid supplementation: 

Administration of essential fatty acids (EFAs) has received a lot of attention in the 

field of small animal dermatology with many publications endorsing the benefits of 

various combinations of omega 3 and omega 6 fatty acids at various dose rates in the 

management of allergy in both cats and dogs. These products may modify the 

arachidonic acid inflammatory cascade, diverting pathways away from the 

production of pro-inflammatory eicosanoids (prostaglandins, thromboxanes, 

leukotrienes) and leading to production of less inflammatory or inhibitory mediators 

such as PGE1. LTB5, PG-2 series, TxA3 and hydroxyeicosapentanoic acid (HEPE). 

EFAs also have been shown to optimise skin barrier function in dogs and have been 

shown to have an additive effect with antihistamines and a significant steroid-sparing 

effect in atopic dogs. 

There are a small number of publications concerning the use of EFAs in horses. An 

open study of 14 horses with insect bite hypersensitivity that were given 20g daily of 

52 


an 80:20 mixture of evening primrose oil and cold water marine fish oil for a 

minimum of 3 months gave promising results, with 4 horses better and 5 horses 

much better than at the beginning of the study and 4 horses no better. However, the 

double-blind placebo controlled trial subsequently conducted failed to demonstrate 

any significant reduction in disease in the treated group (Craig et al 1997). Similar 

results were obtained in a double-blinded cross-over study with omega-3 fatty acid 

supplementation (Friberg and Logas 1999). However, a more recent study of 

flaxseed supplementation in horses with Culicoides hypersensitivity reported reduced 

skin test reactivity, concurrent with a significant decrease in the hair content of longchain 

fatty acids (O'Neill et al 2002). 

In spite of the lack of supportive controlled data in horses, many clinicians feel that 

EFA supplementation is beneficial in some horses. The product DVM Derm Caps 

100s given at doses of 1capsule per 50-100kg bodyweight is reported to be well 

tolerated and effective in some horses. 

Botanical extracts: 

The use of plant and herb extracts in the management of canine atopic dermatitis 

has received attention over recent years, with the development of a product 

containing three plant extracts, derived from tradition Chinese remedies for human 

atopic eczema (Phytopica). Whilst the author is unaware of any published data of 

trials of plant extracts in the management of allergic horses, there is anecdotal 

evidence of the benefits of oral administration of aloe vera liquid extract - doses of 

150ml per horse per day suggested. 

Topical therapies: 

Regular bathing of atopic and insect-bite hypersensitive horses can be very helpful in 

alleviating and ameliorating clinical signs. Products which may be useful include 

colloidal oatmeal shampoos, either alone or in combination with other “soothing” 

products such as aloe vera extract. Moisturisers can also be helpful. For localised 

lesions witch hazel sprays and aloe vera gel extracts can be beneficial. In cases with 

secondary infection and/or secondary seborrhoea, there are products with antiseptic 

properties (chlorhexidine, chloroxylenol, ethyl lactate, benzoyl peroxide) and 

keratoplastic properties (salicylic acid, tars, benzoyl peroxide) that may be 

appropriately utilised. 

Author's experience: 

The outcome in the series of 24 cases discussed previously (Littlewood et al 1998) 

serves to illustrate the author's personal experience in the management of equine 

atopic dermatitis. Advice was given regarding changes to management and feeding 

practices in an attempt to avoid or limit exposure to implicated allergens, with 

additional advise regarding insect avoidance where appropriate. Where management 

changes were insufficient to secure resolution or adequate improvement in clinical 


signs antihistamines (hydroxyzine hydrochloride at an initial dose of 300 mg twice 

daily) were given by mouth or oral prednisolone at a dose rate of 1 mg/kg initially 

daily, reducing to alternate day therapy. 

Follow-up information was obtained for all except one case. Two horses died shortly 

after referral before any response to management alterations could be assessed. 

Progress reports were obtained initially one and three months after referral and 

subsequently at various intervals for up to four years. All cases improved 

considerably after management alterations that were recommended on the basis of 

the history and positive skin test reactions had been implemented. Drug therapy was 

necessary in only six cases. In four cases oral antihistamines were employed 

intermittently when the pruritus or urticaria were severe, often coincident with 

pollination times. A fifth was treated with antihistamines initially, but therapy was no 

longer required after a major change of management. Low dose steroid therapy was 

given to the sixth case initially, due to the severity of the urticaria and angioedema. 

Major management changes were not possible and this horse required ongoing 

intermittent administration of antihistamines because of recurrent urticaria, although 

he remained asymptomatic most of the time. The respiratory problem in this case 

has also persisted and worsened. 

The author has used immunotherapy in only a handful of cases, where it has been 

felt to be of benefit, but the results of management modification are usually 

sufficient to control the problem sufficiently that clients rarely request 

immunotherapy. 

References: 

Craig JM et al (1997) A double-blind placebo-controlled trial of an evening primrose 

and fish oil combination versus hydrogenated coconut oil in the management of 

recurrent seasonal pruritus in horses. Veterinary Dermatology 8, 177 

Fiberg CA & Logas D. (1999) Treatment of Culicoides hypersensitive horses with 

high-dose N-3 fatty acids: a double-blinded crossover study. Veterinary Dermatology 10, 

117. 

Littlewood JD, Paterson S, & Shaw SC. (1998) Atopy-like skin disease in the horse. 

Advances in Veterinary Dermatology 3, p563 

O'Neill W, McKee S & Clarke AF (2002) Flaxseed (Linum usitatissimum) 

supplementation associated with reduced skin test lesional area in horses with 

Culicoides hypersensitivity. Canadian Journal of Veterinary Research 66, 272-7 

54 


Clinical approach to the horse with 

pastern dermatoses 


Crusting and scaling lesions affecting the skin of the distal limb of horses presents a 

diagnostic and therapeutic challenge to the equine practitioner and dermatologist 

alike. The use of various colloquial descriptive terms such as “greasy heel”, 

“scratches” and “mud fever”, which horse owners frequently view as a definitive 

diagnosis, further serves to confuse the issue. At best, these terms should be viewed 

as describing a clinical syndrome, for which there are a number of underlying 

aetiologies. Whilst empirical remedies may be effective in managing such cases, a 

significant number fail to respond to such therapies and can cause frustration to 

client and clinician alike, as well as being a significant welfare problem to the patient 

in some instances. The efforts of the attending clinician should be directed towards 

identifying underlying predisposing factors and pathogens and implementing specific 

therapy to eliminate the problem. Appropriate samples taken at the outset will 

minimise the risk of a chronic, recurrent skin problem whose features may be 

changed by the intervening therapy, making it harder to reach a definitive diagnosis 

later. The client is more likely to be impressed by attempts to make a proper 

diagnosis at the outset, so that correct treatment can be initiated and, hopefully, 

resolution achieved sooner. 

There are a number of factors that may predispose to grease heel syndrome, 

including genetic factors such as presence of feathers in heavy breeds and nonpigmented 

skin; environmental factors such as moisture, prevailing climate and 

management practices; and iatrogenic factors including tack items and topical 

preparations, which are frequently utilised by horse owners. Primary causes of grease 

heel syndrome include physical and chemical irritants and infectious agents such as 

mites and dermatophytes. The extremities may be affected by extreme cold 

(frostbite) and ultraviolet light exposure may result in photodermatoses in nonpigmented 

limbs. Bacterial infection is common in grease heel syndrome, but 

whether this represents a true primary pyoderma or, as in the dog, a secondary 

phenomenon, is not clear. Progressive pathology with fibrosis is a particular problem 

of diseases of the distal equine limb and chronic lesions may be characterised by 

irreversible changes. 

The differential diagnosis for crusted papules, often with “paintbrush” tufting or 

matting of hair, includes dermatophilosis, dermatophytosis and staphylococcal 

(pastern) folliculitis. Cytological preparations are invaluable and are often diagnostic 

in acute, exudative lesions, with causal organisms identifiable in impression smears 

of underside of scabs or crusts. Bacterial and/or fungal culture are helpful in 

identifying actual species involved, although it should be noted that Dermatophilus 


congolensis is not easy to isolate, particularly from older, longstanding lesions. 

However, typical organisms may be seen in wet preparations made from crusts after 

rehydration and maceration on slides, prior to staining. Dermatophilosis is often a 

problem of a number of horses in a yard and may be endemic, with increased 

numbers of affected animals noted in the winter months. The spores are persistent 

in the environment and careful attention to management practices is an important 

part of control measures. Ideally an area should be set aside for topical treatment of 

affected animals and crusts carefully disposed of and the area disinfected. Systemic 

antibiotic therapy is usually effective in cases not responding to topical antibacterial 

agents, but should be continued beyond clinical cure. 

Dermatophytosis can be caused by a number of fungal organisms. Identification of 

the causal agent may be helpful in identifying the original source (other horses, cattle, 

cats, sylvatic species, geophilic). There is also a zoonotic risk to be considered. Scalp 

brushes provide a useful tool for sampling animals for culture, equivalent to the 

Mackenzie toothbrush technique employed in small animals. Management of this 

condition is covered later. 

Pastern folliculitis may be a primary pyoderma, but mixed growth of organisms is 

frequently obtained on swabs. Tissue samples obtained by biopsy may well be a 

better material for culture and provide a truer picture of the major pathogen 

involved. However, cytological examination often provides sufficient information to 

initiate antibacterial therapy. Management of bacterial folliculitis is the subject of a 

later presentation. 

Chorioptic mange is the major parasitic cause of skin lesions of the distal limb. The 

parasite exhibits a preference for heavy breeds of horse. An epidemiological study 

conducted by the author has shown that the presence of feathers is not a 

prerequisite, but the actual nature of the nutritional or other factors provided by 

such horses is unknown. Management of this condition is covered later. 

Harvest mite larvae (“chiggers”) can parasitise the lower limbs of horses grazed on 

pastures inhabited by the free-living adult mites or ridden through infested woods or 

trails. The larval stage requires a blood meal and any convenient mammal may be 

bitten. The larva is only attached for 48-72 hours, but in some horses lesions of 

pruritus, crusting, erythema and scaling may persist beyond detachment of the 

parasite, suggesting a hypersensitivity component to the lesions. Fipronil has been 

demonstrated to be effective in the management of trombiculidiasis in dogs, and 

would be appropriate for the condition in equine patients too, as an off-label use. 

Photosensitivity may affect the distal limbs of horses with white socks. The cause 

may be due to ingestion of primary photosensitising agents, such as hypericin in 

Hypericum spp. of plants (St John’s Wort). Photocontact dermatitis may occur. In the 

case of primary photocontact or systemic photosensitisation, one would expect 

several of a group of horses to be affected, although photoallergic reactions may 

occur, which would be limited to sensitised individuals. Often it is difficult to 

56 


identify plants in a pasture that might be implicated. It has been observed that some 

pastures rich in clover may be associated with cases of photodermatitis in some 

seasons, possibly associated with high rainfall and lush growth, but the exact nature 

of the agent remains obscure. Secondary, hepatogenous, photosensitisation occurs 

when pre-existing liver damage results in failure to metabolise chlorophyll effectively 

and presence of photoactive phylloerythrin in the circulation. The commonest cause 

of chronic liver damage in such cases is poisoning resulting from ingestion of Seneccio 

spp (ragwort), but mycotoxins have also been implicated. The prognosis for cases 

with underlying liver pathology is poor, but cases of primary photodermatitis 

respond to removal from the source of photoactive agent and ultraviolet light 

exposure and appropriate symptomatic therapy of lesions. 

A condition characterised histologically by vasculitis, which appears to be 

photoactivated, has been described. The nature of the underlying aetiology remains 

to be elucidated, but such cases usually respond well to glucocorticoid therapy and 

protection from further ultraviolet light exposure. This entity may well underlie some 

of the cases of so-called “canon keratosis” described in the literature. It is clear that 

this syndrome is not due to urine splashing in intact stallions (“stud crud”) since it 

occurs in females too. As ever, there are some cases of crusting lesions of the distal 

limbs that defy attempts to make a definitive diagnosis and are termed idiopathic. 

Lesions of the coronary band present a distinct range of differential diagnoses. The 

use of various and sundry topical hoof products may be associated with irritant or 

allergic reactions of the coronary band. Dermatophytosis may be restricted to this 

region. Congenital dystrophies are described. Acquired lesions of the coronary band 

can be seen in pemphigus foliaceus, which in the older horse is not infrequently 

confined to the coronary bands. Lesions may also affect the ergots and chestnuts 

and the oral mucosa may be involved. The prognosis for complete cure of such cases 

is poor, but most cases appear to respond to immunosuppressive therapy with 

glucocorticoids and long-term remissions can be achieved, with return to useful 

work. 

Chronic selenosis due to ingestion of plants with high selenium content, or 

accidental misformulation of concentrate feeds results in a coronitis and abnormal 

hoof growth. Loss of mane and tail hair are other features, together with weight loss 

and unthriftiness. Prognosis is dependent upon the severity of lesions, with the hoof 

deformity and pain seen in some cases necessitating euthanasia. 

Coronary band lesions with a histological appearance similar to that seen in 

hepatocutaneous syndrome have been encountered in horses with severe liver 

pathology. The coronary band is frequently involved in the rare condition of 

exfoliative eosinophilic dermatitis and stomatitis/enteritis syndrome, which carries a 

grave prognosis. 


In many cases of coronary band disease a definitive diagnosis can be made on 

histological examination of biopsy material. The optimum method for procuring 

tissue is by the shave biopsy technique, whereby a tangential incision is made over 

the curve of the bulbs of the heel, under regional nerve block and sedation, if 

necessary. Haemostasis is achieved by application of a dressing and pressure 

bandage. Healing is usually uneventful, without any adverse effect on hoof wall 

growth. 

58 


Equine sarcoidosis 


These notes include findings from cases in a multi-centred study collated by Dr Christine Loewenstein, Dr 

Sonya Bettenay and Dr Ralf Mueller,with co-investigators Dr Janet Littlewood, Dr Wayne Rosenkrantz, 

Dr Claudia von Tscharner, Dr Fernando Ramiro-Ibanez and Dr Sherry Myers 

. 

Equine sarcoidosis (generalized or systemic granulomatous disease) is a rarely 

reported disease characterized clinically by multifocal to generalized exfoliative 

dermatitis and histologically by prominent multinucleated giant cell granulomas (also 

occur in up to 50% cases in other organ systems). Equine sarcoidosis has been 

named after the human sarcoidosis syndrome, so named because of these 

characteristic “naked” granulomas. It should not be confused with the far more 

common “equine sarcoid”, which is a fibroblastic tumorous lesion with various 

clinical presentations. 

Only few reports about equine sarcoidosis are published. Since the first published 

case (Anderson and others 1983) there have been only 6 reports with a total of 10 

cases (Duell and others 1997, Heath and others 1990, Peters and others 2003, Rose 

and others 1996, Sellers and others 2001, Woods and others 1992) and several 

general review articles (Mullowney 1985, Scott 1988, Scott 1991, Scott 1992, 

Stannard 1987, von Tscharner and others 2000). All of the reported cases showed 

signs of general disease such as apathy, fever, weight loss or lymphadenopathy. 

Four of the horses died or were euthanized and underwent post mortem 

examination. They had involvement of internal organs including brain, lung, heart, 

lymph nodes, liver, kidney, pancreas, thyroid and adrenal glands (Anderson and 

others 1983, Peters and others 2003, Sellers and others 2001, Woods and others 

1992). Eight horses showed dermatologic symptoms such as scaling, crusting, 

alopecia and nodules (Duell and others 1997, Heath and others 1990, Rose and 

others 1996, Sellers and others 2001, Woods and others 1992). 50% of 8 horses 

recently presented (Spiegel 2005) were said to have pulmonary involvement. 

These findings are in contrast to the human disease where skin lesions are present in 

only 16 to 36% of the cases (Braverman 1998). Pulmonary lesions, however are 

most common and seen with 90% of the patients (Braverman 2003). Human 

sarcoidosis is a multisystemic disease characterised by sarcoidal granulomas. 

Sarcoidal granulomas may also be associated with foreign bodies. They are discrete, 

round to oval and composed of epithelioid histiocytes and multinucleated giant cells 

with very occasional lymphocytes. This is in contrast to typical granulomas which are 


surrounded by a sparse rim of lymphocytes. Thus, the granulomas are referred to as 

"naked" in appearance (Weedon 2002). In horses, the sparsity of lymphocytes is a 

common feature of dermal granulomas and is not emphasized by a special 

nomenclature. 

In a recent retrospective study we asked pathologists and dermatologists world wide 

to contribute cases. Clinical inclusion criteria were the presence of a generalised or 

multifocal, scaling, crusting dermatitis with or without systemic signs and with no 

evidence of a concurrent infectious agent. Histopathologic inclusion criteria were 

defined as diffuse granulomatous inflammation with an infiltrate dominated by 

macrophages and multinucleated giant cells, and negative fungal stains and/or 

cultures. Seven horses were included in this study based on dermatologic and 

histopathologic inclusion criteria. 

Equine sarcoidosis is a rarely reported disease (Sellers and others 2001, Stannard 

1987) and although dermatologists and dermatopathologists from around the world 

were contacted, only 7 cases were obtained which satisfied our inclusion criteria. 

Age of onset ranged from 7 months to 17 years with a mean age of 8 years. This is 

consistent with previously published data, indicating a predisposition for middleaged 

horses (mean age of 9 years in 10 horses reported). In 5/7 cases the breed was 

specified (Quarter horse, Irish hunter and Selle francaise). Comparing to previously 

reported breeds (Anderson and others 1983, Duell and others 1997, Heath and 

others 1990, Peters and others 2003, Rose and others 1996, Sellers and others 2001, 

Woods and others 1992) (1 crossbred, 3 thoroughbred, 1 quarterhorse, 1 hunter, 1 

welsh pony cross, 1 Warmblood, 1 miniature pony, 1 standardbred), Quarter horses 

seem to be overrepresented in our study, but due to the various sources of patients, 

statistical significance could not be verified. 

Previous reported cases included 3 females and 7 males (Anderson and others 1983, 

Duell and others 1997, Heath and others 1990, Peters and others 2003, Rose and 

others 1996, Sellers and others 2001, Woods and others 1992). In our study males 

were overrepresented (6/7), indicating an emphasis of the male gender. However, 

the number of cases is too small to conclude gender predisposition. 

Onset of the disease in our study was generally rapid ranging from weeks to a few 

months. Only one case exhibited clinical signs for longer than 6 months which is in 

accordance to previous reports where one case with sudden worsening of the 

condition after 1 year was described (Heath and others 1990). In human sarcoidosis, 

either an abrupt onset over weeks or an insidious development over months is 

possible (Braverman 1998). 

Scaling, crusting, alopecia and papules in various combinations were the 

predominant lesions. This confirms previous reports (Duell and others 1997, Heath 

and others 1990, Rose and others 1996, Scott 1988, Sellers and others 2001, von 

Tscharner and others 2000, Woods and others 1992). Cutaneous nodules were 

60 


described as a possible feature of the disease (Scott and others 2003, Stannard 1987) 

and were found in one horse (Woods and others 1992). Nodules were identified in 

one horse in this study but were presumed to be injection reactions rather than part 

of the disease. This is in contrast to human medicine, where prevalent lesions are 

papules, nodules, plaques, subcutaneous tumours and scaly erythema (Braverman 

2003). Edema at various body sites (lips, eye lids, distal limbs, ventral abdomen and 

prepuce) was reported previously (Anderson and others 1983, Heath and others 

1990, Peters and others 2003, Woods and others 1992) and was noted in one of our 

horses. Erosions and ulcers described in an earlier report (Sellers and others 2001) 

were seen in 2 horses in our study. In human sarcoidosis, violaceous plaques are 

commonly observed lesions. In some of these, large telangiectatic vessels are present 

on the surface. Inflammatory changes involving these vessels may be the 

pathomechanism responsible for the development of edema, erosions and ulcerative 

lesions in horses. Depigmentation on the lips and eyelid margins was described 

previously (Heath and others 1990). In one of our horses, depigmentation was 

observed at the prepuce. Loss of skin pigmentation is an uncommon manifestation 

in human sarcoidosis, reported to occur exclusively in black patients and may be 

related to decreased melanization of the overlying epidermal cells (Braverman 2003). 

In the literature only one report gives information about the localisation of the initial 

skin lesions manifesting as a swelling around the lips (Anderson and others 1983). 

One author describes the disease onset on the face or limb (Scott 1988, Scott and 

others 2003). This could not be confirmed by the findings of our study, as all horses 

exhibited initial lesions over the trunk and/or shoulder. 

Equine sarcoidosis is reportedly characterized clinically by multifocal to generalized 

exfoliative dermatitis with internal organ involvement and a poor to guarded 

prognosis (Anderson and others 1983, Peters and others 2003, Scott and others 

2003, Sellers and others 2001, von Tscharner and others 2000, Woods and others 

1992). Granulomatous lesions have been reported in lymph nodes, lungs, heart, liver, 

spleen, kidneys, gastrointestinal tract, adrenal and thyroid glands and brain. Affected 

horses typically develop a wasting syndrome and signs of other organ involvement 

such as dyspnoea, gastrointestinal or central nervous signs or lameness (Anderson 

and others 1983, Heath and others 1990, Peters and others 2003, Rose and others 

1996, Sellers and others 2001, Woods and others 1992). In this study, only one horse 

exhibited clinical signs of systemic disease such as intermittent fever, prescapular 

lymphadenopathy, depression, poor body condition, and nasal discharge. However, 

no internal tissue specimens were taken to further investigate internal organ 

involvement. As the horse actually responded clinically to glucocorticoid therapy, an 

infectious origin seems unlikely, but confirmation of granulomatous changes in 

organs other than the skin was not made. 

The low incidence of systemic signs seen in horses included in this study could have 

been influenced by our inclusion criteria. We contacted dermatologists rather than 

internists with the request for participation, which may have led to a bias for horses 

with predominant skin disease rather than horses affected with severe systemic 

disease evaluated by internists rather than dermatologists and the search criterion in 


the pathology labs was for granulomatous skin. Recently, a group of 7 horses were 

investigated which had primary pulmonary disease and no reported concurrent 

dermatologic symptoms (Pusterla and others 2003). All of these horses showed 

granulomatous lesions in the lungs, which formed the inclusion criterion for the 

report. Cutaneous signs may not have been present, not mentioned specifically or 

overlooked due to the gravity of the systemic disease. There may be significant 

similarity between human and equine sarcoidosis and the disease may present with a 

spectrum of clinical signs. Dermatologic lesions may be on one end of the spectrum 

and pulmonary lesions on the other. 

Sarcoidosis is a rare disease in equine medicine and the pathogenesis is unclear. In 

human medicine, histopathologic findings of sarcoidosis resemble those seen in 

tuberculosis. Furthermore, tuberculosis shows an increased incidence in patients 

with sarcoidosis. As long as 35 years ago, a role for atypical mycobacteria was 

presented (Mankiewicz 1964). By using molecular biologic methods, DNA from M. 

tuberculosis and an unidentified nontuberculous mycobacterium was identified in 

tissue sections and bronchial washings of some patients with sarcoidosis (Fidler and 

others 1993). Multiple species of mycobacteria were detected by polymerase chain 

reaction (PCR) predominantly from samples of the lymph nodes and pulmonary 

tissue (Li and others 1999). These findings support a potential role of mycobacteria 

in the pathogenesis of sarcoidosis in some human patients. However it must not be 

thought to be the exclusive infectious agent as recent studies in Japan and Europe 

suggest that Propionibacterium spp. may also be involved in the aetiology of sarcoidosis 

(Eishi and others 2002). Infectious agents could not be detected in horses by culture, 

electron microscopy, animal inoculation, direct immunofluorescence or 

immunoperoxidase testing (Heath and others 1990, Scott 1991, Stannard 1987, von 

Tscharner and others 2000). In three previously reported cases positive titers to 

Borrelia burgdorferi were shown (Rose and others 1996). In a recent report, paraffinembedded 

skin specimens from 8 horses with sarcoidosis were evaluated with special 

stains and PCR assays for Mycobacteria spp., Borrelia burgdorferi, Coccidioides immitis, 

Cryptococcus neoformans and Corynebacterium pseudotuberculosis to no avail (Spiegel and 

others 2005). There are anecdotal reports about improvement of the condition in 

horses which were moved from one state to another (personal communication Tony 

Stannard). It was hypothesized that the beneficial effect of relocation was due to 

differences in environmental concentrations of mould spores which may play a role 

in the pathogenesis of the disease. None of the horses included in this study had a 

correspondent history. 

In humans, massive immunosuppressive doses of glucocorticoids are the treatment 

of choice for sarcoidosis with significant systemic involvement (Braverman 2003). 

Cutaneous lesions generally respond to therapy for systemic involvement, but often 

recur when the dosage is lowered or discontinued. Patients without systemic 

involvement are typically not treated with glucocorticoids. There are anecdotal 

reports of success with chloroquine (Zic and others 1991), hydroxychloroquine 

(Jones and others 1990), methotrexate (Lower and others 1995), minocycline 

(Bachelez and others 2001), thalidomide (Calderon and others 1997, English and 

62 


others 2001), isotretinoin(Waldinger and others 1983), allopurinol (Pollock 1991), 

levamisol (Veien 1986) and tranilast (Yamada and others 1995), but controlled 

studies are lacking. Many of these agents have immunomodulating properties. 

Treatment with penicillin, sulfonamid/trimethoprim and doxycyclin was without 

beneficial effect. All but one horse responded to administration of 

prednisolone/prednisone, typically at 1.0 to 1.5 mg/kg -1 q24h for 1 to 6 weeks 

followed by a gradual dose reduction. Alternative therapy to glucocorticoids (as 

advocated in human cutaneous disease) has not been evaluated in horses. Five of the 

seven horses were still alive one year after diagnosis; one was still alive 8 months 

after diagnosis and then lost to follow up. In two horses, prednisolone led to 

complete remission, but clinical signs initially recurred after cessation of therapy. 

These two horses went into remission again with reintroduction of treatment. 

Overall, 4/ 6 known horses are still alive 1 to 8 years after diagnosis without any 

treatment. This seems to indicate a fair to good prognosis for horses with cutaneous 

sarcoidosis. Based on previous reports, concurrent systemic signs indicate a guarded 

prognosis. However, the only horse in our study with systemic signs responded to 

glucocorticoid administration. None of the horses in our study died within one year. 

In previously reported cases, deterioration was rapid and occurred within a few 

weeks. We may indeed have a skewed sample selection, but it just may be possible 

that early presentation and treatment with glucocorticoids prevented generalisation 

of the disease in our cases. 


References 

1. Anderson, C.A. and Divers, T.J. (1983) Systemic granulomatous 

inflammation in a horse grazing hairy vetch. Journal of the American 

Veterinary Medical Association 183, 569-570 

2. Bachelez, H., Senet, P., Cadranel, J., Kaoukhov, A. & Dubertret, L. (2001) 

The use of tetracyclines for the treatment of sarcoidosis. Archives of 

Dermatology 137, 69-73 

3. Braverman, I.M. (1998) Skin Signs of Systemic Disease. 3rd edn. 

Philadelphia, W.B. Saunders. pp 373-376 

4. Braverman, I.M. (2003) Sarcoidosis. In Fitzpatrick´s Dermatology in General 

Medicine. 6th edn. Eds I.M. Freedberg, A.Z. Eisen, K. Wolff, K.F. Austen, 

L.A. Goldsmith and S.I. Katz. NewYork, McGraw-Hill. pp 1777-1783 

5. Calderon, P., Anzilotti, M. & Phelps, R. (1997) Thalidomide in dermatology. 

New indication for an old drug. Journal of the American Academy of 


6. Duell, U., Wernitz, U., Onderka, J. & Andres, F. (1997) Sarkoidose - eine 

seltene Autoimmunerkrankung bei einem Pferd. Praktischer Tierarzt 78, 486- 

490 

7. Eishi, Y., Suga, M., Ishige, I., Kobayashi, D., Yamada, T., Takemura, T., 

Takizawa, T., Koike, M., Kudoh, S., Costabel, U., Guzman, J., Rizzato, G., 

Gambacorta, M., du Bois, R.M., Nicholson, A.G., Sharma, O.P. & Ando, M. 

(2002) Quantitative analysis of mycobacterial and propionibacterial DNA in 

lymph nodes of Japanese and European patients with sarcoidosis. Journal of 

Clinical Microbiology 40, 198-204 

8. English, J.C., Patel, P.J. & Greer, K.E. (2001) Sarcoidosis. Journal of the 

American Academy of Dermatology 44, 725-743 

9. Fidler, H.M., Rook, G.A., Johnson, N.M. & McFadden, J. (1993) 

Mycobacterium tuberculosis DNA in tissue affected by sarcoidosis. British 

Medical Journal 306, 546-549 

10. Heath, S.E., Bell, R.J., Clark, E.G. & Haines, D.M. (1990) Idiopathic 

granulomatous disease involving the skin in a horse. Journal of the American 

Veterinary Medical Association 197, 1033-1036 

11. Jones, E. and Callen, J.P. (1990) Hydroxychloroquine is effective therapy for 

control of cutaneous sarcoidal granulomas. Journal of the American 

Academy of Dermatology 23, 487-489 

64 


12. LeGall, F., Loeuillet, L., Delaval, P., Thoreux, P.H., Desrues, B. & Ramee, 

M.P. (1996) Necrotizing sarcoid granulomatosiswith and without 

extrapulmonary involvement. Pathology Research and Practice 192, 306-313 

13. Li, N., Bajoghli, A., Kubba, A. & Bhawan, J. (1999) Identification of 

mycobacterial DNA in cutaneous lesions of sarcoidosis. Journal of 

Cutaneous Pathology 26, 271-278 

14. Lower, E.E. and Baughman, R.P. (1995) Prolonged use of methotrexate for 

sarcoidosis. Archives for Internal Medicine 155, 846-851 

15. Mankiewicz, E. (1964) The relationship of sarcoidosis to anonymous 

bacteria. Acta Medica Scandinavica Supplement 425, 68-73 

16. Mullowney, P.C. (1985) Dermatologic diseases of horses Part V: Allergic, 

immune-mediated and miscellaneous skin diseases. Compendium of 

Continuing Education for the practicing Veterinarian 7, 217-228 

17. Panciera, R.J., Mosier, D.A. & Ritchey, J.W. (1992) Hairy vetch (Vicia villosa 

Roth) poisoning in cattle: update and experimental induction of disease. 

Journal of Veterinary Diagnostic Investigation 4, 318-325 

18. Peters, M., Graf, G. & Pohlenz, J. (2003) Idiopathic systemic granulomatous 

disease with encephalitis in a horse. Journal of Veterinary Medicine, series A- 

Physiology Pathology Clinical Medicine 50, 108-112 

19. Pollock, J.L. (1991) Sarcoidosis responding to allopurinol. Archives of 


20. Pusterla, N., Wilson, W.D. & Magdesian, K.G. (2003) Investigation of the 

etiology and immunologic characterization of "idiopathic granulomatous 

pneumonia" in seven horses admitted to the VMTH from 1975-2001. 

http://www.vetmed.ucdavis.edu/ResServ.html 

21. Rose, J.F., Littlewood, J.D., Smith, K. & Shearer, D. (1996) A series of four 

cases of generalized granulomatous disease in the horse. In Advances in 

Veterinary Dermatology III. Eds K.W. Kwochka, T. Willemse and C. von 

Tscharner. Boston, Butterworth-Heinemann. pp 562-563 

22. Scott, D.W. (1988) Immunologic diseases. In Large Animal Dermatology. 

Philadelphia, W.B. Saunders. pp 326-328 

23. Scott, D.W. (1991) Unusual immune-mediated skin diseases in the horse. 

Equine Practice 13, 10-15 


24. Scott, D.W. (1992) Diagnostic des dermatoses inflammatoires équines 

:analyse de la modalité de réaction histopathologique:étude personelle 

portant sur 315 cas. Point Vétérinaire 24, 245-248 

25. Scott, D.W. and Miller, W.H. (2003) Miscellaneous skin diseases. In Equine 

Dermatology. New York, Elsevier Health. pp 675-680 

26. Sellers, R.S., Toribio, R.E. & Blomme, E.A. (2001) Idiopathic systemic 

granulomatous disease and macrophage expression of PTHrP in a miniature 

pony. Journal of Comparative Pathology 125, 214-218 

27. Spiegel, I.B., White S.D. et al. (2005) Retrospective study of cutaneous 

equine sarcoidosis and potential underlying infectious etiologies. 20th 

Proceedings of North American Veterinary Dermatology Forum, 166. 

28. Stannard, A.A. (1987) Generalized granulomatous disease. In Current 

Therapy in Equine Medicine. 2nd edn. Eds N.E. Robinson. Philadelphia, 

W.B. Saunders. pp 645-646 

29. Strickland-Marmol, L.B., Fessler, R.G. & Rojiani, A.M. (2000) Necrotizing 

sarcoid granulomatosis mimicking an intracranial neoplasm: 

clinicopathologic features and review of the literature. Modern Patholology 

13, 909-913 

30. Veien, N.K. (1986) Cutaneous sarcoidosis: prognosis and treatment. Clinical 

Dermatology 75-87 

31. von Tscharner, C., Kunkle, G. & Yager, J. (2000) Stannard´s illustrated 

equine dermatology notes. Veterinary Dermatology 11, 161-223 

32. Waldinger, T.P., Ellis, C.N., Quint, K. & Voorhees, J.J. (1983) Treatment of 

cutaneous sarcoidosis with isotretinoin. Archives of Dermatology 119, 1003- 

1005 

33. Weedon, D. (2002) Skin Pathology. 2nd edn. London, Churchill Livingstone. 

pp 194-195 

34. Woods, L.W., Johnson, B., Hietala, S.K., Galey, F.D. & Gillen, D. (1992) 

Systemic granulomatous disease in a horse grazing pasture containing vetch 

(Vicia sp.). Journal of Veterinary Diagnostic Investigation 4, 356-360 

35. Yamada, H., Ide, A., Sugiura, M. & Tajima, S. (1995) Treatment of cutaneous 

sarcoidosis with tranilast. Journal of Dermatology 22, 149-152 

36. Zic, J.A., Horowitz, D.H., Arzurbiaga, C. & King, L.E.J. (1991) Treatment of 

cutaneous sarcoidosis with chloroquine. Archives of Dermatology 127, 1034- 

1040 

66 


Introduction 

The equine sarcoid: an update 

Reg Pascoe 

A locally aggressive fibroblastic tumour which is probably the most common 

cutaneous tumour found in horses. Prevalent in horses aged between 1-6 

years.(Torrentegui & Reid 1994: Pascoe & Knottenbelt 1999) The lesions are 

frequently not life threatening but they can severely limit the use of the horse and 

reduce its sale prospects, however euthanasia is not uncommon due to the 

prolonged nature of treatment, likelihood of recrudescence of the problem and cost 

The role of a virus, in particular Bovine papillomavirus (BPV), in its cause and 

transmission is still uncertain Population and family studies have shown an 

association between sarcoid susceptibility and MHC class II alleles (Lazary et al., 

1985, 1994) 

Some research indicated there were no mutations of the somatic tumour suppressor 

p53 gene in either horses or donkeys associated with the development of sarcoids 

More recently somatic p53 gene mutations have been found to be associated with 

the development of some sarcoid tumours in donkeys (Nasir et al 1999). BPV-DNA 

was detected in 88% and 91% of the successful swabs and scrapings from sarcoids 

respectively. The overall diagnostic sensitivity of the technique was significantly 

lower compared to the clinical diagnosis of sarcoids and is unsuitable for occult 

sarcoids. However, the detection of BPV-DNA in all samples obtained from 

sarcoids with an ulcerated surface opens new perspectives for the detection of 

sarcoid involvement in wounds or recurrence after sarcoid removal.(Martens et al 

2001) 

In a further study BPV DNA was detected in essentially all sarcoids examined 

(96/98) it was also detected in normal skin samples from the horses with sarcoids 

suggesting the possibility of a latent viral phase. Viral latency may be one explanation 

of the high rate of recurrence following surgical removal. All tissues from healthy 

horses with non sarcoid neoplasms or papilloma were negative to BVP DNA ( Carr 

et al 2001) 

Lesions occur in locations which are prone to injury and some have a history of 

previous skin wounds. There is also strong presumptive evidence that sarcoids can 

be transmitted by biting and domestic flies which feed on sarcoid tissue and then 

browse on other horses with open sores, wounds or tumours. The introduction of a 


horse with fibroblastic sarcoids can result in the appearance of sarcoids in other 

previously uninfected horses on the farm within 6-8 months. 

The distribution of lesions varies with type of sarcoid and geographical location. The 

para-genital region is most frequently and the limbs least affected in the UK. In 

Queensland (Australia) the majority of lesions occur on the head, neck and limbs 

and very rarely in the para-genital region (Pascoe & Summers (1981). A recent study 

of sarcoid cases in the UK showed single and small numbers of sarcoids (2-8 

sarcoids per horse) were uncommon, whereas 10 to several thousand are more 

common. The majority of lesions seen in UK horses are occult or verrucous, with at 

least six major types described (Knottenbelt et al 1995) 

The distribution of the six types show great variation with a preponderance of 

fibroblastic tumours occurring in the para-genital area; in Australia almost all leg 

sarcoids are a fibroblastic type. Sarcoids have a high capacity to invade the dermis 

and subcutis. True metastatic dissemination does not appear to occur. Sarcoids can 

occur in fresh healing wounds in previously normal horses, or re-occur at the same 

site following apparent complete surgical removal. 

Six clinical entities: 

1.Verrucous (warty) type 

Definition 

These tend to be slow-growing and not very aggressive until injured in some fashion, 

e.g. biopsy, rubbing. poor surgical removal 


Wart-like growth on and above skin, may be sessile or pedunculated. 

Slow growing. Trauma to surface may convert them to a fibroblastic reaction. 

(Pascoe 1990) 


Papillomatosis, chronic blistering, hyperkeratosis (chronic sweet itch), equine 

sarcoidosis (chronic granulomatous disease) squamous cell carcinoma. 

Diagnosis 

Biopsy: preferably total wide excision followed by cryotherapy 

2.Fibroblastic type 

Definition 

A more aggressive tumour, particularly when located on the lower limbs and 

coronet. 

68 



Small fibrous nodule in skin. Erosion or injury leads to excessive granulation tissue 

growth. Lateral progression by local invasion. Metastasise rarely if at all. 

difficulty lies in the determination of normal and infected granulation tissue 

regrowth after tumour removal 


Exuberant granulation tissue, habronemiasis, neurofibroma / neurofibrosarcoma, 

botryomycosis, fibrosarcoma, squamous cell carcinoma, pythiosis, sweat gland 

tumour. 

Diagnosis 

Biopsy should include normal skin as well as tumour. 

3.Mixed Verrucous and Fibroblastic type 

Definition 

Progressively more aggressive as changes from verrucous to fibroblastic type. 


Probably a progressive state from a verrucous type. Contains both verrucous and 

fibroblastic elements 


The presence of more than one form of sarcoid is almost self-diagnostic. 

4.Occult type 

Definition 

Hairless areas which contain one or more small cutaneous nodules. 


Loss of hair. Often roughly circular. Very slow growing until injured. Presence of 

one or more hard shot-like nodules in the skin from 2-5mm diam. Nodules may 

progress to warty verrucous growth or if injured, develop into fibroblastic lesions. 

Commonly around mouth, eyes, neck and body 


Dermatophytosis (ringworm), blisters, burns. 

Diagnosis Clinical picture. Remember biopsy may convert lesion into active 

fibroblastic sarcoid. 


5.Nodular type 

Definition 

Occurs as subcutaneous nodules and when these erode the overlying skin, they 

become more aggressive fibroblastic type tumours 


Subcutaneous spherical nodules usually under normal skin(5-20mm). Most 

frequently found in the groin or eyelid area Skin may become thin over larger 

nodules. Where ulceration occurs, lesion quickly develops into fibroblastic sarcoids. 


Fibroma, neurofibroma, equine eosinophilic granuloma, melanoma, collagen 

necrosis (axilla - rare), dermoid cysts. 

Diagnosis 

Biopsy: total excision if possible with wide margins 

6.Malevolent type (Knottenbelt DC, et al 1995)) 

Definition 

A recent variation of sarcoids showing increased malignancy with a suggestion of 

metastasis adjacent to the initial site. 


Invasive sarcoid. Infiltration of lymphatics. Multiple tumours locally to metastatic 

sarcoid in other lymph nodes. May follow surgical interference to sarcoids in jaw and 

elbow region. Cords of tumour extend in lymphatics. 


Squamous cell carcinoma, subcutaneous mycosis, lymphangitis, glanders, enzootic 

lymphangitis, cutaneous histoplasmosis. 

Diagnosis 

Clinical change to original sarcoid. Invasiveness of regrowth. 

Reaffirmation of diagnosis of sarcoid from new invasive tissue. 

General management consideration 

Due to the uncertain outcome in 100% of cases, the horse owner should be very 

aware of the seriousness of the problems which can arise from this disease. 

Treatment should involve a full discussion of treatment options, on the likelihood of 

successful treatment, and at worst, the likelihood of prolonged or repeated treatment 

which, while the condition is contained, may not fully resolve it. 

70 


Assessment should be made on the following grounds: 

1. The value of the animal - actual or sentimental. 

2. Previous treatment and history, i.e. likelihood of chronic granulation tissue 

from old wire cuts or refractory granulation. 

3. The cost of each avenue of treatment and the likelihood of a successful 

outcome to that type of treatment, i.e. repeated single local medication may 

eventually be much more expensive than surgical removal, radiation therapy 

or cryosurgery. 

4. If at all possible, the results of biopsy should be known before the final 

prognosis is given. 

5. Likelihood of further spread of the condition if treatment is: 

(i) not undertaken 

(ii) delayed 

(iii) not correct. 

6. The possibility of a contagious nature of the sarcoid and the further 

transmission to other horses in the group. 

Overview of modalities for treatment of sarcoids 

1. Ligatures 

Elastrator rings, lycra or even heavy elastic bands can be used. Application 

can easily be made, even on fractious horses, using a twitch or tranquillizer. 

This works best on single sarcoids where loose skin on body or neck is 

available to allow proper placement of ligature. 

2. Local medication 

Moderately successful on single small sarcoids: 

- use of podophyllin 50% applied daily for > 30 days. 

- 10% arsenic trioxide in aqueous solution for 5 days. Causes heavy 

scab formation which may be difficult to remove. 

- 5-fluorouracil applied under a bandage.(Roberts 1970) 

3. Vaccination or stimulation of immune system 

Bovine wart vaccine has been used and found to be valueless. 

Pox vaccines used into the actual sarcoid lesion were also unsuccessful. 

Autogenous vaccines have been manufactured but results have not been 

good: recovery in under 25% of animals treated (Wheat 1964, Page & Tiffany 

1967). In 1977 the use of BCG vaccine was reported. Lesions were injected 

with BCG vaccine, 1ml at 7-10 day intervals, and a good response claimed for 

this type of treatment (Wyman et al 1977). A similiar type treatment was made 

using a non-living wall preparation from BCG vaccine which was injected at 

intervals of 2-4 weeks. Anaphylaxis had been reported following the use of 

the living BCG vaccine due to proteins produced from the metabolized 

vaccine bacteria causing the production of antibody which react when further 


72 

treatment is given. 

This danger was overcome by the use of a BCG cell wall vaccine preparation 

which was as effective as the living BCG vaccine but does not have the 

adverse side effects of producing anaphylaxis (Hepler & Leuker 1980).The 

reported use of such a vaccine (CSL Equoid Australia) for the intradermal 

treatment of sarcoid gave favourable results with 1-2 injections 14-21 days 

apart in 80% of the cases treated.(Vaneslow et al 1988). Production problems 

with this vaccine led to its permanent withdrawal from the market in 1993. 

4. Surgical treatment 

Surgical excision– removal of sarcoid, under local or general anaesthetic, plus 

at least 15-20mm ring of normal. Disadvantages: 50% may return and as 

wound heals may spread to other areas on the horse; removal of large areas 

of normal skin precludes closure and slowshealing time; inability to remove 

this quantity of skin from leg lesions increases risk of return 

CO2 Laser Complete ablasion for small Sarcoids id very successful large 

tumours can be less well ablated and may reoccur 

5. Electrocautery 

Where single small masses are involved ordinary cautery is satisfactory but reoccurrence 

can be expected. With large electrocautery units, both cutting and 

fulguration are available and should be used: remove tumour by cutting 

current then treat area, particularly the skin edges, with fulguration to 

desiccate tissue. 

6. Cryosurgery 

Useful for Sarcoids. Complications are under or over treatment; injury to 

surrounding blood vessels, nerves, bone and tendon. The success of 

cryotherapy depends on correct technique.(Fretz & Barbour 1987) 

Cryonecrosis therapy - The success or otherwise of cryotherapy rests in 

proper observation of correct technique. The following summary assists in 

understanding the modality and its side effects. 

Cryosurgery summary 

(i)Select adequate 'heat' sink (best is liquid N2) 

(ii)Freeze tissues rapidly to below -20C 

(iii)Allow slow thaw to +36C 

(iv)Repeat cycle 2-3 times 

(v)Restrict circulation to area using tourniquet 

(vi)Protect surrounding tissue with Polystyrene 

(vii)Hair follicles are destroyed by double cycle 

(viii)Vitiligo occurs with a single freeze thaw cycle; scars with double cycle 


(ix)Bone becomes devitalized if included in freeze/thaw cycles; regeneration 

may take 2 years 

(x)Deep infiltrative tumours are seldom satisfactorily treated by cryosurgery 

(xi)Eliminate bulk by surgical trimming before freezing 

Technique summary 

(i)use of thermocouple 

(ii)use of 2 cycle freeze and thaw 

(iii)freeze adequately 

(iv)protect normal tissue if using liquid spray 

(v)assess patient's temperament and use the correct restraint 

(vi)give Tetanus antitoxin or Toxoid booster 

(vii)give full explanation of the process and after-care to the owner 

(viii)do not fail to tell the owner about white hair formation 

7. Radiation therapy 

Can either be a large distant irradiating source (Teletherapy) which restricts 

the use to a limited number of large facilities; or (Brachytherapy) treatment 

with implants or isotopes to the tumour which is more practical for equine 

treatments.(Blackwood & Dobson 1994, Theon 1998, Knottenbelt & Kelly 

2000, Henson & Dobson 2004) 

Squamous cell carcinoma, sarcoids, soft tissue sarcomas (fibrosarcoma, 

haemangiosarcoma and neurofibromas), cutaneous lymphomas and 

melanoma are suitable for successful treatment. 

Advantages 

less disfigurement, better therapeutic success 

and as a follow-up to failed surgery, cryosurgery or immunotherapy. 

Best results come with debulking surgery under general anaesthesia 

previous debulking leads to residual activity of dividing tumour cells which 

are most susceptible to radiation and to lowered isotope cost due to smaller 

treatment area. 

Disadvantages- 

requires the presence of a specialist radiologist or radiophysicist 

special secure areas for use of hospitalised horses 

training of personnel to use care around treated horses 

increased costs due to isotopes, general anaesthetic 

and longer hospitalization in specialized accommodation 

Isotopes 

Strontium 90 and Radon 222 (Fraunfelder et al 1982a,b), Iodine 128, Caesium 

137 and Gold 198 (Wyn Jones 1979,1983) and Iridium 192 (Turrel et al 1985) 


74 

In practical terms, those commonly used are iridium 192 and gold 198 which 

are both gamma emitters. 

Strontium 90, a beta particle emitter has a limited penetration of 3mm, so it's 

use is restricted to those tumours following very careful debulking or to cleanup 

surface cells in conjunction with implants. When applied to the target area 

following post surgical ablation of the tumour, Strontium 90 in an applicator 

has been successfully used for some sarcoids and ocular squamous cell 

carcinoma 

8. Photodynamic Therapy 

The therapeutic potential of the photodynamic compound, hypericin, in the 

treatment of equine sarcoids has been evaluated.In vitro cytotoxicity on three 

equine cell lines to phototoxic effect was comparable to that on different 

highly sensitive human cell lines and significantly influenced by the energy 

density used although independent of the cell type. 

In vivo anti tumoural action of photodynamic therapy using hypericin was 

used experimentally on three equine sarcoids in a donkey. With either a 0.3% 

hypericin solution in polyethylene glycol (PEG400)/H2O L/L. or a 0.3% 

hypericin solution in DMSO/H2O L/L was used. 

Intratumoural injections were performed every 5days under short acting GA. 

Mean dosage of hypericine was 0.7mg/cm3 tumoural tissue. Tumours were 

illuminated over 30 min each day with a light delivery by a KL 1500 cold light 

source at 1 cm distance from the surface (results in an energy density of 72 

J/cm2.) . However, this is only for a total of 25 days. 

81% reduction in tumour volume was obtained at the end of therapy and 2 

months later, a 90% reduction was observed. Further experimental work 

should be performed, but these results suggest that photodynamic therapy 

using hypericin has a potential for the non-invasive treatment of equine 

sarcoids. (Martens 2000) 

9. Radio frequency hyperthermia 

This modality has been used in equine sarcoid and squamous cell carcinoma 

and is most successful in small tumours Reports of treatments indicate repeat 

treatments are common and the method is not gained wide acceptance 

10. Chemotherapy 

Many and varied compounds of inorganic tissue poisons such as arsenic, 

mercury and antimony, and their combinations have been used to treat 

sarcoids. More recently podophyllin, methotrexate, 5-fluorouracil, cisplatin 


and mitomycin C have been used. All require some form of repeat treatment 

medication, many on a daily basis for as long as 30 days. Our results are 

similar to those of the Liverpool Veterinary School, UK using AW-3-LUDES 

a 80% recovery rate with emphasis on initial treatment success as being a 

peculiarity of the drug combination ( Knottenbelt & Walker 1994). Repeat 

treatment and treatment of previously treated unresolved lesions is likely to 

be less successful but still more likely than other compounds and treatments 

commonly used. 

Persistence and client compliance are important for the likelihood of higher 

success rates. 

11. Electro chemotherapy 

Enhances the effectiveness of chemotherapeutic agents all treatments were 

given under short General anaesthesia. An intra tumoral drug Cisplatin in oil 

is injected into the lesion. After 5mins two electrodes are placed over the 

tumour using a conductive paste and short, intensive electrical pulses (8 

pulses 0.1ms at 1-Hz frequency with 1.3 kV voltages) are applied to increase 

the permeability of the tumour cell membrane to achieve higher cell 

concentrates of the injected drug. 

It works most satisfactorily on small tumours( 10cm tumours were found to be best 

treated after de bulking and given multiple electro treatments simply by 

overlapping and shifting the electrodes. Eradication so far has been 

successful in all treated horses in under four treatments (Tamzali et al.2003) 

Prognosis 

Varies from good to poor depending on the site, number and type of lesions, and 

their response to initial treatment.Good client understanding is important for final 

resolution 


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Turrel JM, Stover SM & Guorgyfalvy J (1985) - Iridium-192 interstitial brachytherapy 

of equine sarcoid: Vet Radiol 26:20-24 

Vaneslow BA, Abetz I and Jackson ARB (1988) - BCG emulsion immunotherapy of 

equine sarcoid; Equine vet J (1988) - 20(6)444-447 

Wheat JD (1964) - Therapy for equine sarcoids; Mod vet Prac 45:62 

Wyman et al (1977) Immunotherapy of equine sarcoid: a report of 2 cases J Am Vet 

Assoc 171 :449 

Wyn-Jones G (1983) - Treatment of equine cutaneous neoplasia by radiotherapy 

using iridium 192 linear sources; Equine vet J 15:361-365 


Introduction 

78 

Histopathological review of 

equine sarcoids 


Jenny Charles 

The sarcoid is the most common skin tumour of horses, donkeys and mules and is a 

locally invasive fibroblastic neoplasm which lacks metastatic potential. Individual 

animals may have multiple tumours, either synchronously or sequentially. Although 

spontaneous regression of equine sarcoids after a protracted growth period has been 

reported, it is a rare occurrence and most lesions require surgical excision, 

cryosurgery, immunotherapy, radiation brachytherapy or other intervention. Local 

recurrence of sarcoids is common and is expected of incompletely excised lesions. 

There is considerable evidence implicating papillomaviruses (closely related to 

bovine papillomaviruses types 1 and 2) in the aetiopathogenesis of equine sarcoids. 

Gross appearance 

Most sarcoids are grossly characterised by firm dermal thickening by cream-white 

tissue with thickening, roughening and hyperkeratosis of the skin surface. The 

tumour may be sessile, domed or pedunculated and well demarcated or poorly 

circumscribed. The surface of protruberant sarcoids is commonly ulcerated. The 

gross appearance of many sarcoids may closely mimic that of exuberant granulation 

tissue and, in ulcerated tumours, granulation tissue may coexist with neoplastic tissue 

and contribute to lesion growth. 

Various classification schemes have been proposed by equine clinicians based upon 

the gross appearance of sarcoids. These schemes are essentially for descriptive 

purposes. The gross appearance of sarcoids may alter over time, both as part of 

neoplastic progression and in response to lesion abrasion, ulceration or iatrogenic 

trauma. The anatomic location of a sarcoid may also influence its gross appearance. 

Six variants have been described: occult, verrucous, fibroblastic, nodular, mixed and 

malevolent. 

Occult sarcoids emerge as one or a few, well-defined, annular areas of hair loss 

with variable scaling or crusting. These lesions, which may closely resemble those of 

dermatophytosis or focal frictional injury, may gradually expand or remain static for 

months or years before ultimately evolving into firm dermal or subcutaneous 

nodules or relatively sessile, hyperkeratotic verrucous lesions. Abrasion or surgical 

biopsy of occult sarcoids may provoke vigorous fibroblastic proliferation and 

emergence of a more aggressive fibroblastic variant. Occult sarcoids may occur at

any anatomic location but commonly arise on the medial thigh, prepuce, neck and 

face. 

Verrucous (warty) sarcoids are usually less circumscribed than occult sarcoids and 

protrude as palpable masses due to an increased dermal neoplastic component. 

They may be sessile or pedunculated. The degree of overlying hyperkeratosis and 

scaling is variable but there is often a partially or totally alopecic, dry, cauliflower-like 

surface. This variant is also relatively slow-growing but a more aggressive 

fibroblastic type may emerge following trauma. Verrucous sarcoids need to be 

distinguished from squamous papillomas induced by equine papillomavirus and from 

chronic frictional irritation. Verrucous sarcoids are most commonly located in the 

axillary and inguinal areas. 

Fibroblastic sarcoids involve both the dermis and subcutis, with the extent of deep 

dermal and subcutaneous infiltration often being underestimated on clinical 

examination. This variant typically manifests as a protruberant, firm to fleshy, 

ulcerated mass which closely resembles exuberant granulation tissue. It is wellvascularised 

and prone to bleed when minimally traumatised. Most sarcoids arising 

on the brisket or limbs are of fibroblastic appearance. Fibroblastic sarcoids may 

enlarge rapidly over weeks to months and then stabilise and persist for years. 

Differential diagnoses for such lesions include, in addition to proud flesh, squamous 

cell carcinoma, botryomycosis, habronemiasis, phycomycosis, fibrosarcoma and 

peripheral nerve sheath tumour. 

Nodular sarcoids usually involve only the subcutis as one or multiple, spherical, 

mobile nodules usually covered by intact skin of normal appearance. Intradermal 

nodular sarcoids may occasionally be seen and the overlying skin may appear thin 

and shiny. Sarcoids involving the palpebral margins are typically nodular and this 

variant is also commonly found on the medial thigh, prepuce and inguinal area. 

Nodular sarcoids, being well demarcated, are amenable to surgical excision but 

incomplete excision (or traumatic ulceration of the overlying skin) may encourage 

emergence of a more aggressive fibroblastic variant. Nodular sarcoids may grossly 

resemble nodular necrobiosis (equine eosinophilic collagenolytic granuloma) and 

other mesenchymal tumours such as melanoma, fibroma or peripheral nerve sheath 

tumour. 

Mixed sarcoids present with a combination of the gross characteristics of two or 

more of the verrucous, fibroblastic and nodular forms and may represent a 

transitional phase as a more rapidly growing and locally aggressive neoplasm emerges 

from a previously stable focus. Mixed sarcoids are most commonly found in the 

axillary and inguinal areas and on the face. 

Malevolent sarcoids are rare, highly invasive variants which infiltrate along 

lymphatics to produce nodular cording and multiple ulcerated fibroblastic nodules. 

The neoplastic tissue may extend along lymphatics to involve regional lymph nodes. 

Most malevolent sarcoids have been observed following intereference with a 


fibroblastic variant, particularly on the elbow or jaw. Differential diagnoses for such 

lesions include various forms of chronic infectious lymphangitis/lymphadenitis (e.g. 

glanders, epizootic lymphangitis and cutaneous histoplasmosis) and metastasising 

carcinomas. 

Why biopsy? 

Histopathology usually permits confirmation of a clinical diagnosis of equine sarcoid 

and elimination of the considerable list of differential diagnoses. However, nonexcisional 

biopsy may provoke transition of a quiescent sarcoid into a rapidly 

growing aggressive one. For this reason, many equine practitioners are loath to 

interfere, particularly with large or poorly demarcated lesions or when a suitable 

method of treatment is unlikely to be available once the diagnosis is confirmed. 

Diagnostic histological features of equine sarcoids 

Histologically, most sarcoids are characterised by dermal fibroblastic proliferation 

and intimately associated, pseudoepitheliomatous hyperplasia of the epidermis. 

There is usually some degree of hyperkeratosis and there may be mild parakeratosis. 

Long, narrow, anastomosing rete pegs of hyperplastic and at least focally acanthotic 

epidermis extend into the proliferating spindle cell component in the dermis. 

The infiltrative and poorly demarcated dermal component is usually of moderately 

high cell density, with the superficial portion tending to be more cellular than the 

deep part. The dermal fibroblasts are slender to plump fusiform cells with poorly 

defined cytoplasmic boundaries. The nuclei may be slender and elongate or enlarged 

and of irregular shape. Mitotic figures are usually infrequent (0-1 per high power 

field) but may be more numerous (up to 2-3 per high power field) in superficial than 

in deep areas of sarcoids and adjacent to areas of ulceration. Mitoses and 

fibroblastic nuclear pleomorphism, anisokaryosis and nucleolar enlargement may be 

observed in rapidly growing or recurrent sarcoids; cellular anaplasia is, however, rare. 

The fibroblasts are typically arrayed in tight whorls, interweaving bundles, haphazard 

tangles and occasionally herringbone and basket weave patterns, with a small to 

moderate amount of intercellular collagen. In recently developed sarcoids, the 

volume of intercellular collagen may be minimal. In chronic lesions, the collagen 

content increases and the dense fibres may appear hyalinised. Plump dermal 

fibroblasts usually directly abut the epidermis and, in a high percentage of sarcoids, 

are characteristically oriented perpendicular to the epidermal basement membrane in 

a picket-fence arrangement. Hair follicles enveloped by fibroblasts may undergo 

cystic dilation. 

Histological variants 

Prominent hyperplasia of the epidermis with formation of long rete pegs is not 

invariably present in sarcoids. It is usually observed in verrucous and mixed forms 

and at the margins of ulcerated areas in fibroblastic sarcoids. In occult sarcoids, the 

80 


epidermis may be histologically normal, minimally hyperplastic or atrophic; 

hyperkeratosis, if present, is often mild. Epidermal thinning is a common finding in 

nodular sarcoids but the epidermis may be normal if the fibroblastic component is 

confined to the subcutis or involves the dermis but does not directly underrun the 

epidermis. 

All sarcoids are characterised by an increased density of fibroblasts but occult 

sarcoids are usually less cellular than other forms. Some occult sarcoids are 

characterised by only a subtle increase in the density of fibroblasts in the superficial 

to mid dermis and a localised reduction in the number of adnexal structures. The 

fibroblasts are frequently not in typical whorling patterns or oriented as 

subepidermal picket-fences in occult tumours. Picket-fence alignment is also 

commonly absent in nodular sarcoids. 

In some sarcoid variants, hyperplasia of the epidermis is more pronounced than the 

dermal fibroblastic proliferation. These variants may histologically mimic a 

squamous papilloma. 

Non-diagnostic biopsies 

Excisional biopsies are more likely to be diagnostic than are punch biopsies, 

particularly if the excisional biopsies are histologically sectioned perpendicular to the 

skin surface to reveal the epidermal component of the lesion and the epidermaldermal 

interface. If punch biopsies are taken, it is important to avoid ulcerated or 

superficially inflamed areas in which diagnostic features may be obliterated or 

obscured. 

The typical epidermal component of sarcoids may not be demonstrable in ulcerated 

lesions. In the absence of a hyperplastic epidermis, the dermal component of the 

sarcoid may be misdiagnosed as granulation tissue, a fibroma, a fibrosarcoma or a 

peripheral nerve sheath tumour. Superficial dermal fibroblast proliferation may also 

be obliterated by ulceration or obscured by granulation tissue in traumatised lesions. 

Differential diagnoses 

Sarcoids are usually readily distinguished from squamous papillomas histologically by 

virtue of their dermal fibroblastic component. 

Granulation tissue may be present within ulcerated sarcoids and is characterised by 

orderly proliferation of both fibroblasts and endothelial cells, with the new capillaries 

aligned in parallel and at right angles to the fibroblasts and new collagen fibres. A 

maturation face may be apparent in older granulating lesions, with collagen of low 

cellularity in deeper areas and ongoing fibrovascular proliferation superficially. 

Fibromas can be distinguished from sarcoids by being expansively growing, well 

circumscribed nodules which compress adjacent structures. They are mainly 


composed of collagen with only small numbers of fibroblasts/fibrocytes of normal 

morphology and only rarely are mitotic figures visible. Histological differentiation of 

sarcoids and fibrosarcomas may be more problematical; however, anaplasia of 

fibroblasts is rarely observed in sarcoids and perpendicular alignment of fibroblasts 

beneath the epidermis is not expected in fibrosarcomas or other mesenchymal 

neoplasms. Histological detection of close association of a spindle cell tumour with 

a peripheral nerve or its sheath may be useful in identifying peripheral nerve sheath 

tumours. 

Alternative diagnostic methods 

With the advent of polymerase chain reaction (PCR) technology, there is the 

potential for rapid diagnosis of equine sarcoids by identification of bovine 

papillomaviral DNA in swabs or scrapings of the surface of suspected lesions. In 

one study of 92 sarcoids, the overall sensitivity of this test was 88% for swabs and 

91% for scrapings, with all sarcoids having partially or completely ulcerated surfaces 

being correctly identified. The swab technique was found to be unsuitable for occult 

sarcoids due to low sensitivity. 

PCR amplification of bovine papillomaviral sequences can also be performed on 

formalin-fixed, paraffin-embedded tissues to confirm a diagnosis of equine sarcoid 

when histopathological examination of biopsy material is inconclusive. 

82 


References 

D.C. Knottenbelt, S. Edwards and E. Daniel. Diagnosis and treatment of the equine 

sarcoid. In Practice 1995; 17: 123-129. 

D.C. Knottenbelt and R.R. Pascoe. Colour Atlas of Diseases and Disorders of the Horse. 

Wolfe Publishing, Barcelona, 1994: pp. 275-279. 

A. Martens, A. De Moor, J. Demeulemeester and R. Ducatelle. Histopathological 

characteristics of five clinical types of equine sarcoid. Res. Vet. Sci. 2000; 69:295-300. 

A. Martens, A. De Moor and R. Ducatelle. PCR detection of bovine papilloma virus 

DNA in superficial swabs and scrapings from equine sarcoids. Vet. J. 2001; 161:280- 

286. 

E. Marti, S. Lazary, D.F. Antczak and H. Gerber (eds.). Report of the first 

international workshop on equine sarcoid. Equine vet. J. 1993; 25:397-407. 

R.R. Pascoe and D.C. Knottenbelt. Manual of Equine Dermatology. W.B. Saunders 

Company Ltd., London, 1999: pp. 244-248. 

J.N. Tarwid, P.B. Fretz and Clark, E.G. Equine sarcoids: a study with emphasis on 

pathologic diagnosis. Comp. Contin. Educ. 1985; 7:S293-300. 

I.F. Williams, A. Heaton and K.G. McCullagh. Connective tissue composition of 

the equine sarcoid. Equine vet. J. 1982; 14:305-310. 


84 

How I treat: equine bacterial 

folliculitis 



The diagnosis of bacterial folliculitis in the horse will be made typically based on the 

clinical lesions, frequently with supportive cytology and bacterial culture. Less 

frequently a biopsy will be performed. 

Clinical presentation: 

Varies depending on the underlying predisposing cause. It occurs frequently 

secondary to trauma and maceration, less commonly to an underlying disease and is 

most commonly seen in spring and summer. Bacterial folliculitis is also a frequent 

complicating factor of Dermatophytosis. Lesions are often painful which can have 

interesting consequences when the affected area is in the saddle and/or tack area. 

Indeed the pain (or rather the horses response to it!) is often the driving reason for 

the consultation and need for therapy. 

The most common initial lesions include papules, pustules, crusted papules and 

larger crusts. These may not be observed until there are actual fissures and/or ulcers 

with larger crusts. However they may be detected early in animals which are 

groomed daily. Urticaria with small follicular papules is a common early 

presentation of some horses, which can be confused as an uncomplicated allergy. 

These early cases will frequently respond to symptomatic steroid therapy, only to 

relapse again once the anti-inflammatory component of the treatment has stopped. 

They may also show a slightly more prolonged clinical response to a topical 

combined antibiotic-steroid agent…. But have a higher relapse rate as these topicals 

do not always reach the deeper affected areas of the follicle. 

Medication Choices: 

Bacterial folliculitis in the horse is most frequently caused by coagulase-positive 

staphylococci. This is a “deep” pyoderma, which will typically not self resolve and 

so antibacterial therapy is an essential part of any treatment regime. Clipping and 

cleaning, topical antibacterial agents and systemic antibiotics are frequently all 

utilised and even then the lesions may take quit some time (weeks to months) to 

resolve. Superficial pyodermas can, at least initially, be treated empirically. If 

appropriate therapy does not resolve the condition, a culture and sensitivity is

indicated. Each sample for culture and sensitivity should be accompanied by 

cytologic examination and culture results interpreted in light of the cytology, as 

growth of different microorganisms does not indicate necessarily that they are 

present in significant numbers in vivo. 

A bacterial culture and sensitivity is almost always indicated when treating horses 

with a deep pyoderma, however whether the owners will elect to pursue this without 

an initial empirical trial therapy is another question. Therefore we frequently make a 

“best guess” when using systemic antibiotics. Whilst Streptococcus equi or 

Corynebacterium pseudotuberculosis are the most common organisms found in abscesses, 

Streptococci and coagulase-positive staphylococci and are most commonly seen with 

folliculitis. 

Local geographic use of antimicrobials does lead to a geographic variation in 

resistance (and sensitivity) rates, so that extrapolating a report from Colorado to 

Queensland or even Sydney to Brisbane is not necessarily useful and may even be 

counterproductive. Similarly a horse stabled in (for example) a busy racing stable, 

with multiple animals and a frequently changing population which is intensively 

husbandried in Melbourne, may have quite a different bacterial population than one 

in the Dandenongs which is not stabled, lives alone, retired in a paddock with a few 

sheep. They may both have a coagulase-positive staphylococcus, but the resistance 

patterns may have more to do with husbandry and immediate environment, than 

with significant geography. 

The intensity of investigation and treatment will, as always in veterinary medicine, be 

to a large part determined by the owner finances, expectations and abilities to 

undertake recommended treatment regimes. 

1. Shampoo therapy. Shampoo therapy can provide effective medical and 

cosmetic management of dermatoses. However, shampooing the whole 

body of a horse is a major undertaking and thus shampoo therapy is most 

commonly used for localized skin disease. Fungal and bacterial 

infections, allergies as well as mane and tail seborrheas are the most 

common indication for shampoo therapy in equine practice. There are 

few adverse effects associated with shampoo therapy, although they are 

recognized. However, shampoo therapy is a symptomatic treatment, and 

rarely "cures"a dermatosis. Chlorhexidine (frequency q 1-14 days) is 

useful in horses as it is not inactivated by organic matter and tends to be 

not irritating or drying. Benzoyl peroxide (frequency q 7-14 days) is a far 

more potent antibacterial agent. Degreasing (and thus drying), 

keratolytic. In horses with dry or normal skin, a moisturizer must be used 

after the shampoo! It may be irritating, particularly in concentrations 

over 3%. Iodofors (frequency q 7-14 days) are typically used by every 

horse owner as the first step prior to calling the vet, they are antifungal, 

antibacterial, viricidal and sporicidal. They may also be helpful in 

decreasing environmental contamination with fungi. 


86 

2. Topical antibacterials: are not listed here, almost every veterinarian will 

have their own “favourite”. The combination of antibiotic with a low 

penetration steroid is frequently a helpful treatment modality. The 

inflammatory response can be exuberant in horses and can actually 

complicate the resolution of the foliculitis. It can also play a particularly 

helpful role in those horses which have allergies as an underlying 

predisposing cause. 

3. Macrolids such as erythromycin and lincomycin may cause severe 

diarrhea due to their effects on bacterial flora in the large colon. 

Tetracyclines also should be used with caution. 


Proper dosage and proper duration are important for the success of antibacterial 

therapy. Although many bacterial infections in the horse respond to short courses of 

antibiotics, longer courses may be needed in particular if the folliculitis has extended 

to a furunculosis. The likelihood of this occurrence increases with the duration of 

the (untreated) disease and also with the pathogenicity of the causative agent(s). For 

example it is more likely to occur early in a dermatophyte associated folliculitis than 

an allergic, non-traumatised one. 

Selected antibiotics in equine dermatology: 

Drug 

Formulation Indications 

Adverse effects Dose 

Penicillin G 300,000 Infections with most gram-positive and Hypersensitivity 20,000-40,000IU/kg (10 ml/70- 

IU/ml for gram-negative cocci (not penicillinase- reactions 150 kg bodyweight) IM q 12h 

injection producing strains), Clostridium sp., 

Fusobacterium and Actinomyces. 

Penicillin V 500-mg Infections with Actinomyces, most Gastrointestinal 40-60 mg/kg (10 tablets/100kg 

tablets spirochetes and Gram-positive and signs with oral bodyweight) q 8 h 

Gram–negative cocci, which do not administration, 

produce penicillinase. 

hypersensitivity 

reactions 

Trimethoprim/ 800mg Infections with Gram-positive bacteria Transient 20-30 mg/kg (1 tablet/30-50 kg 

sulfadiazine 

trimethoprim (streptococci, staphylococci). Many pruritus, bodyweight) q 12-24 h; 15-20 

/ 160mg Gram-negative organisms of the family diarrhea, mg/kg (10 ml/250-350 kg 

sulfadiazine, Enterobacteriaceae are also susceptible hypersensitivities bodyweight) IV q 12-24 h 

48% sterile (but not Pseudomonas aeruginosa). ,blood dyscrasias 

Chlor-amphenicol 

injection 

1000mg Infections with most gram-positive and Bone marrow 50 mg/kg q 8 h (10 tablets/200 

tablets, 100 gram-negative cocci, Clostridium sp., toxicity 

kg bodyweight) 

mg/ml 

sodium 

succinate 

as Fusobacterium and Nocardia. 

powder 

injection 

for 

Cephalexin 1000-mg Infections with streptococci, Vomiting and 20-30 mg/kg q 8 h 

tablets staphylococci,Actinobacillus, 

diarrhea; very 

Corynebacteria (except C. equi) 

rarely 

excitability, 

tachypnea or 

Enrofloxacin 136-mg 

blood dyscrasias 

Cartilage 2.5-5 mg/kg q 24 h 

tablets 

erosions 

growing foals 

in 

Taken from, with permission, Equine Dermatology Made Easy, 

Teton New Media, author Dr Ralf Mueller. 


Treatment Regime: 

This varies with a number of factors, some of which will be more important than 

others in different individuals: 

1. Site 

88 

1. Site 

2. Affect on the horse 

3. Affect to the owner (is it a show horse?) 

4. Response (or lack of) to previous therapy 

5. Extent (area) and severity (depth) of the lesions 

6. Owners ability to treat / manage 

7. Environmental conditions 

8. Monies available for therapy 

I associate various sites with various possible underlying causes and as such, the 

treatment regime will include a treatment modality aimed at the presumed, or 

diagnosed underlying cause, as well as addressing the folliculitis. 

Tack areas: such as underneath bridle cheek straps, girths, saddles, cruppers. These 

areas have a naturally thicker skin than many other areas and so frequently the 

folliculitis +/- associated furunculosis will require a longer course of systemic 

antibiotics. I do not expect these infections to heal well without systemic antibiotics 

and also without rest from the presence of the overlying tack. Completely spelling a 

horse for the 3 to 4 weeks the folliculitis may require to resolve can be catastrophic 

from the point of view of a working horse (owner), however I expect that any 

external trauma to these areas during that time will extend the recovery period. 

Lambskin pads, utilising different tack, frequent surface washes may all help to 

minimise this trauma IF the horse must be worked. 

Pastern: frequently associated with environmental maceration, which needs to be 

corrected before one can honestly expect a recovery. However there are the other 

implicated factors such as UV-light and a contact hypersensitivity (whether that is 

mediated through a UV-sensitisation is still discussed). The lower leg swelling 

associated with a lymphadenopathy in “Draught horses” can also be associated 

initially with a pastern folliculitis. 

These are often deep, fissured and associated with a furunculosis which requires 

both topical and systemic therapy for the bacterial component. 

Generalised: may be associated with underlying stress or allergy factors, which will 

ned to be addressed concurrently. Due to the large body area affected, these will 

also require a systemic course, but typically respond fast. 


2. Affect on the horse and 3. Affect to the owner 

The degree with which the dermatitis is interfering with work, the cosmetic 

appearance and the simple well being of the horse will all be factors which affect just 

how intensive the chosen treatment will be. These lesions are frequently painful and 

may turn a placid creature into a demon. If the horse is a work or show horse and 

the lesions are in the tack area, then the consequences are even more dramatic 

Owners will be affected emotionally, by the change in personality of their beloved 

pet, and by the potential inability of their horse to fulfil its “job”. 


90 

How I treat: equine insect bite 

hypersensitivity 


Mandy Burrows 

Insect bite hypersensitivity is the most common allergic skin disease of the horse. It 

has a worldwide distribution. 

Cause and Pathogenesis 

This disorder represents type I (immediate and late phase) and type IV (delayed) 

hypersensitivity to antigens (presumably salivary) from numerous Culicoides (gnats) 

and Simulium (black flies) species, Stomoxys calcitrans (stable fly) and possibly 

Haematobia irritans (horn fly). Some horses have hypersensitivities to multiple insects. 

Culicoides gnats (biting midges, sandflies) are the most important cause of equine 

insect hypersensitivity. Results of gnat collection techniques, intradermal testing with 

gnat antigens and passive cutaneous anaphylaxis trials have incriminated numerous 

Culicoides species in various parts of the world. C.brevitarus (C.robertsi) appears to be 

most important in Australia. In general Culicoides gnats are most active when the 

ambient temperature is above 28C, when humidity is high and when there is no 

breeze. Culicoides gnats breed in standing water and generally fly short distances. 

Clinical evidence strongly suggests that this disorder has familial and genetic 

predispositions. Intradermal injections of Culicoides (and occasionally Simulium, 

Stomoxys and Haematobia) extracts produce immediate (30 mins) and delayed (24 to 48 

hours) reactions in over 80% and about 50% respectively of affected horses. Some 

affected horses also develop late phase immediate (4 to 6 hours) reactions. Affected 

horses typically react to all Culicoides spp injected suggesting shared common 

allergens. Most horses react to two or more genera of insects. 

Clinical features 

No age or sex predilection; most horses first develop clinical signs at 3 to 4 years and 

the condition typically worsens with age. Coat colour is not a risk factor. It may be 

seen in any breed but certain breeds are reported to be at increased risk; Icelandic, 

German Shire, Welsh ponies, Arabians, Connemaras, and quarter horses. Clinical 

signs are distinctly seasonal (spring through to autumn) but in warmer subtropical to 

tropical climates the disease can be non seasonal with seasonal (summer) 

exacerbations. Clinical signs are often worse near dawn and dusk as this is the 

favourite feeding time for many Culicoides species.

Affected horses usually scratch and chew themselves and rub against environmental 

objects (stalls, fences, doorways, posts, trees etc) Reflex nibbling movements can 

often be elicited by manipulation of the skin of the mane. Horses usually show one 

of three patterns of skin disease i.e dorsal, ventral or some combination thereof and 

these differences in lesion distribution probably reflect the different preferential 

feeding sites of the various insect species. 

Dorsal insect hypersensitivity is characterised by pruritus with or without crusted 

papules, usually beginning at the mane, rump and base of tail. The condition then 

extends to involve the face, pinna, neck, shoulder and dorsal thorax. Self trauma and 

chronicity lead to excoriations, variable hypotrichosis and alopecia, lichenification 

and pigmentary disturbances especially melanoderma and melanotrichia. 

Ventral insect hypersensitivity is characterised by pruritus with or without crusted 

papules, beginning on the ventral thorax and abdomen, axillae and groin. The legs 

and intermandibular space are often involved. Secondary changes may occur as 

above. Horses with insect bite hypersensitivity rarely have involvement of the flanks. 

In addition, horses with insect hypersensitivity uncommonly develop urticaria and 

when they do it is typically papular. 

Secondary bacterial folliculitis is not uncommon. Affected horses may suffer 

behavioural changes (anxious, nervous, restless, aggressive) and be unfit for riding, 

showing or working. Some horses will lose weight due to the constant irritation. 

Some horses have concurrent atopic disease or adverse food reactions which can 

greatly complicate the diagnostic work-up and therapeutic management. 

Diagnosis 

The differential diagnosis will vary according to the distribution of lesions. The 

definitive diagnosis is based on history, physical examination, ruling out other 

conditions and response to insect control. 

Intradermal testing with insect extracts, especially Culicoides is usually positive with 

insect hypersensitivity. Reactions may be present at 30 minutes (immediate), 4-6 hrs 

(late phase) and 24-48hrs (delayed) or combinations of these. Normal horses can 

have positive reactions and the prevalence of positive reactions in normal horses 

increases with increasing age. 

Antibodies against Culicoides and Stomoxys have been detected in the serum of 

affected horses by ELISA. Other investigators have found no difference in ELISA 

scores using Culicoides extract between normal horses and horses with insect 

hypersensitivity. The diagnostic value of ELISA results is presently undocumented. 


The typical histologic appearance of insect hypersensitivity is a superficial and deep 

perivascular to interstitial eosinophilic dermatitis with focal areas of infiltrative to 

necrotising eosinophilic mural folliculitis and focal eosinophilic granulomas. These 

changes are not pathognomonic for insect hypersensitivity and may be seen with 

adverse food reactions and atopic dermatitis 

Treatment 

The management of insect hypersensitivity involves insect control and the use of 

topical and systemic antipruritic agents. Treatment of unrugged, grazing horses 

is difficult and frustrating. Secondary bacterial infections must be recognized and 

treated. 

Insect control 

92 

• Stable horses between 4pm and 8am 

• Cover horses with rugs and hoods 

• Use fine mesh screens in stables 

• Spray housing and screens with residual insecticides 

• Install floor or overhead fans in stables 

• Time operated spray mist insecticide systems are useful but expensive 

• Drain lakes, marshes, swamps, irrigation channels 

Fly repellents and insecticides 

• 4% permethrin (Permoxin ® Dermcare Vet Pty Ltd); use a 0.1% solution as 

a spray or rinse daily for 7 days then once a week 

• 0.2% fenvalerate (Sumifly Buffalo Fly Insecticide ® Fort Dodge); use 0.1% 

solution and apply 800ml to 1L on dorsal midline and body every 7 days 

• 0.15% pyrethrin, piperonly butoxide, N-octyl bicycloheptene dicarboxamide, 

di-N-propylisocinchromeronate, citronella (Musca-Ban Insecticidal spray ® 

Country Lfe Animal Health) spray/wipe-on 

• 0.2% pyrethrin, piperonyl butoxide, N-octyl bicycloheptene dicarboxamide, 

di-N-propylisocinchromeronate, diethyltoluamide, (N-Dem spray Insecticidal 

Lotion and Spray ® Joseph Lyddy) 

• 0.2% pyrethrin, diethyltoluamide, N-octyl bicycloheptene dicarboxamide, di- 

N-propylisocinchromeronate, benzalkonium chloride (Fly-Repella cream ® 

Troy Laboratories) 

• Commercial bath oils diluted with equal parts of water has been reported 

anecdotally as a useful leave on repellent 


• Cattle ear tags impregnated with pyrethroids braided into manes and tails and 

attached to halters 

• Maintaining a continuous film of liquid film of mineral oil on paraffin is 

reportedly useful to prevent Culicoides gnats from crawling down the hairs to 

the skin 

Antipruritic therapy 

Topical 

• Cold water 

• Colloidal oatmeal shampoo Episoothe ® Virbac or Aloveen ® Dermcare- 

Vet Pty Ltd 

• 0.2% benzyl benzoate Ectosol ® Troy Laboratories 

Systemic 

Antihistamines have limited effect 

• Chlorpheniramine 0.25 to 0.5mg/kg q 12 hours PO 

• Doxepin 0.5 to 0.75mg/kg q 12 hours PO 

• Amitryptilline 1mg/kg q 12 hrs PO 

Corticosteroids 

• Methyl prednisolone acetate 200mg IM 

• Triamcinolone acetonide 0.02 to 0.04 mg/kg IM 

• Prednisolone 2 mg/kg PO q 24 hrs induction dosage for 5 days reducing to 

1mg/kg q 24 hrs for 5 days reducing to 1mg/kg q 48 hrs 

• Dexamethasone 0.2mg/kg PO q 24hrs induction dosage for 5 days 

reducing to 0.1mg/kg q 24 hrs for 5 days reducing to 0.05 to 0.1mg/kg q 72 

hrs 

Fatty acids 

• Linseed oil 

• Flaxseed oil 

• Commercial fatty acid supplements 

Immunotherapy 

• The usefulness of allergen specific immunotherapy (ASIT) in equine insect 

hypersensitivity is unclear. Early attempts to use immunotherapy were 

reported to be unsuccessful. A few horses that had positive reactions to only 

mosquito or black fly extracts appear to respond well. 

• A small study was conducted using 14 horses in a double-blinded, placebocontrolled 

fashion using an aqueous whole body extract of C.variipenis. There 


94 

was no difference in response to the Culicoides extract compared to placebo 

but the study only lasted 6 months. 

• Another small open study using 10 horses used a whole body C.variipenis 

extract in adjuvant (mycobacterial cell wall fraction). Injections were 

administered subcutaneously every 6 to 10 days for first year then every 

month for the second year. After two years 8/10 horses had moderate to 

complete control of pruritus. This protocol should be repeated in a doubleblinded, 

placebo controlled fashion in a larger number of horses. 

Control 

• Affected animals should not to be used for breeding due to the hereditary 

nature of insect hypersensitivity 

References 

Anderson GS et al: Immunotherapy trial for horses in British Columbia with 

Culicoides hypersensitivity. J Med Entomol 33: 458, 1996 

Barbet JL et al Specific immunotherapy of Culicoides hypersensitive horses: a double 

blind study. Equine Vet J 22:232, 1990 

Brostrom H et al Allergic dermatitis (sweet itch) of Icelandic horses in Sweden: an 

epidemiological study. Equine Vet J 19:229, 1987 

Fadok VA: Culicoides hypersensitivity. In:Robinson NE (ed). Current Therapy in 

Equine Medicine II. WB Saunders Co. Philadelphia, PA, 1987, p 624 

Fadok VA, Greiner EC: Equine insect hypersensitivity: skin test and biopsy results 

correlated with clinical data. Equine Vet J 22: 236, 1990 


How I treat: equine 

pemphigus foliaceus 

Ralf Mueller 

Pemphigus foliaceus (PF) is an autoimmune disease, directed against desmosomes in 

the stratified squamous epithelium, leading to the loss of intracellular cohesion, 

acantholysis and blister formation within the epidermis (Halliwell 1979, Laing and 

others 1992, Scott and Miller 2003). It is the most common equine autoimmune 

skin disease (Scott and others 1987, Von Tscharner and others 2000). The first 

clinical article of pemphigus foliaceus in the horse was published by Barnick and 

Gutzeit in 1891. In 1981, the first histopathologic and immunopathologic 

documentation of equine PF in a horse was reported (Johnson and others 1981). 

The reported age in recent publications varied from 2 months (Laing and others 

1992) to 25.5 years (Zabel and others 2005). Most authors do not report breed, sex 

predilection or seasonality (Scott and others 1983, Pascal and others 1995, Von 

Tscharner and others 2000, Zabel and others 2005). Appaloosas were over 

represented in one study (Scott 1989). 

A retrospective study of 20 cases of equine pemphigus foliaceus reported an 

increased prevalence of disease between September and February (Vandanebeele and 

others 2004). Another recent retrospective study was not able to duplicate these 

findings (Zabel and others 2005). Scott (1989) and White (1992) reported a 

deterioration of disease in warm, humid, and sunny weather. Two horses (13%) in a 

recent case series showed evidence of seasonal disease deterioration. One of these 

horses, a Warmblood, did not show clinical signs during winter and deteriorated 

every summer when it was brought on a high altitude pasture. After the horse was 

kept in the valley permanently, no more clinical signs were noted (Zabel and others, 

2005). Environmental factors such as increased exposure to ultraviolet light may 

have been involved in the pathogenesis. The second horse was a research pony, 

which showed worsening of clinical signs in summer and also related to stress 

(anaesthesia, handling). Pemphigus foliaceus may be triggered by various factors 

such as stress, drug administration, systemic disease or Culicoides hypersensitivity 

(White 1992, Von Tscharner and others 2000), and the disease may wax and wane 

(Fadok 1995). Von Tscharner and others (2000) describe hereditary as well as 

infectious or environmental factors predisposing horses to pemphigus foliaceus, as 

the disease has been noted in unrelated horses living in the same area. The head and 

lower extremities have been reported as commonly affected sites (Von Tscharner 

and others 2000, Scott and Miller 2003). In a report of 8 horses with pemphigus 

foliaceus, a site predilection for the ventrum was found (Scott 1983). The disease 


frequently generalizes within 1-3 months (Von Tscharner and others 2000, Scott and 

Miller 2003). The coronary band may show changes and may be the only affected 

site (Fadok 1995, Von Tscharner and others 2000). Other targets might be the 

prepuce or the mammary glands (Johnson 1997, Scott and Miller 2003). Pitting 

oedema of the lower extremities and the ventral abdomen is seen in over 50% of the 

cases (Manning 1983, Scott 1989, White 1992) and might be the only initial sign of 

disease (Scott and Manning 1983, Schulte and others 1989, Von Tscharner and 

others 2000, Scott and Miller 2003). Urticaria can occur weeks before classical 

lesions such as pustules and/or crusts are seen (Von Tscharner and others 2000). 

Some authors state that horses may occasionally be pruritic, but more often are 

painful (Von Tscharner and others 2000, Scott and Miller 2003), others mention 

pruritus in 50% of the horses (Zabel and others 2005). 

The primary lesions in PF are vesicles, bullae and pustules. These lesions are very 

fragile and short-lived. Most often patients present with secondary lesions such as 

erosions, epidermal collarettes, crusts, alopecia, and scaling (Von Tscharner and 

others 2000, Scott and Miller 2003). Systemic signs like fever, depression, anorexia, 

lethargy and weight loss (Scott 1989, White 1992, Manning 1983), and nonregenerative 

anaemia, neutrophilia, hypoalbuminia, elevated alkaline phosphatase, 

elevated fibrinogen and hyperglobunemia may occur (George 1984, Edmond 1986, 

Day and others 1986, Scott and others 1987). 

Tests useful in the diagnosis of equine pemphigus foliaceus include direct smears, 

skin biopsies and immunofluorescence or immunohistochemical testing (Scott and 

Miller 2003). Cytology from crusted areas or intact pustules may show large 

numbers of neutrophils and acantholytic cells and is reported to be a useful test in 

the diagnosis of equine pemphigus foliaceus. Multiple biopsies from intact pustules 

or crusts are needed to confirm the diagnosis (Von Tscharner and others 2000). 

Primary dermatohistopathologic findings include subcorneal and/or intraepidermal 

pustules, associated with marked acantholysis (Scott 1989, Yaeger and Scott 1993, 

Von Tscharner and others 2000). In the absence of pustules, large numbers of 

acantholytic cells and neutrophils found in the crusts are often the only diagnostic 

finding. As acantholysis may also be seen in dermatophytosis, special stains and 

fungal cultures are recommended (Scott and Miller 2003). Histopathology is 

reported to be far more reliable than immunopathologic testing in the diagnosis of 

equine pemphigus foliaceus. (Scott and others 1984, Day and Penhale 1986, Griffith 

1987, Scott and Miller 2003). 

The prognosis for equine pemphigus foliaceus patients depends on age of onset. 

Younger horses (< 1 year) seem to have a better prognosis, the disease tends to be 

less severe, responds better to treatment and may spontaneously regress or not 

require further medication once in remission (Laing and others 1992, Von Tscharner 

and others 2000, Scott and Miller 2003). However, mature horses (> 5 years) have a 

less favourable prognosis and most require aggressive treatment (Von Tscharner and 

others 2000). Spontaneous remission is rare, but has been reported (White 1992, 

Amory and others 1997, Von Tscharner and others 2000, Scott and Miller 2003). 

96 


Treatment of pemphigus foliaceus in the horse requires immunosuppressive therapy. 

Due to financial reasons, the most commonly used drugs are glucocorticoids (Scott 

and Miller 2003, von Tscharner and others 2000). If prednisone is used and not 

effective, prednisolone or dexamethasone may be used successfully. The reason for 

this may be poor absorption, failure of hepatic conversion, possibly rapid secretion 

or a combination of these factors. Prednisone or prednisolone is given at 1-2 

mg/kg/day, the dexamethasone dose is 0.05-0.1 mg/kg/day. Treatment is altered to 

every other day once patients are in remission and doses may be reduced further 

depending on the individual situation. Long term remission after complete cessation 

of therapy has been reported and seems to be more common in young horses. The 

most feared adverse effect seen with glucocorticoids is laminitis. Corticosteroids 

may alter the flood flow in the hoof causing hypoxia in the lamina. They may also 

have a direct effect on epidermal cell metabolism. If unacceptable adverse effects 

are noted or if the response to glucocorticod treatment is unsatisfactory, 

azathioprine or gold salts may be used. Azathioprine has been used for the 

treatment of immune-mediated skin disease in the horse at a dose of 1 mg/kg/day 

(Scott and Miller 2003). It is associated with bone marrow suppression and 

occasional acute liver toxicity in dogs and humans, however, this has not been noted 

in the horses treated so far. The reason for this lack of adverse effects may be the 

low number of horses treated, poor oral absorption or a more rapid metabolisation 

of the drug in horses. Chrysotherapy is another option for the treatment of equine 

pemphigus foliaceus at a dose of 1 mg/kg IM weekly (Vandenabeele and others 

2004). However, aurothioglucose is currently not available in many countries. Dogs 

frequently develop secondary infections with immunosuppressive therapy. This is 

not seen often in horses. 

The prognosis of equine foliaceus should be given as guarded at first presentation. 

However, in some horses (particularly those with disease onset at young age) therapy 

can be discontinued without recurrence after it resulted in clinical remission, thus we 

always attempt treatment. In patients with financial constraints, glucocortocoids are 

used exclusively for therapy, but azathioprine or aurothioglucose may be used as 

steroid-sparing agents in horses with unacceptable treatment results or adverse 

effects, if owners are willing to accept the higher financial burden. 


References 

AMORY, H., BECO, L., DESMECHT, D., JAQUINET, E., VANDENPUT, S., 

LOMBA, F., (1996) Pemphigus foliace dans l’espece equine: Synthese at description 

de 2 cas. Annales de Medecine Veterinaire 141, 139- 148 

BARNICK, W. & GUTZEIT, R., (1891) Ein Fall von acutem Pemphigus beim 

Pferde. Zeitschrift Veterinär Kunde 3, 241-244 

DAY, M.J., PENHALE, W.J., (1986) Immunodiagnostics of autoimmune skin 

disease in the dog, cat and horse. Australian Veterinary Journal 63 (3), 65-68 

EDMOND, R.J., FREVERT, C., (1986) Pemphigus foliaceus in a horse. Modern 

Veterinary Practice 67, 527-530 

FADOK, V.A., (1995) An overview of equine dermatoses characterized by scaling 

and crusting. Veterinary Clinics of North America: Equine Practice11, 43-51 

GEORGE, L.W., WHITE S.L., (1984) Autoimmune Disease in Large Animals. 

Veterinary Clinics of North America: Large Animal Practice 6, 79- 86 

GRIFFITH, G., (1987) Pemphigus foliaceus in a Welsh Pony. Compendium on 

Continuing Education for the Practicing Veterinarian 9, 347-353 

HALLIWELL R.E., (1979) Skin disease associated with autoimmunity. Veterinary 

Clinics of Northern America: Small Animal Practice 9, 57-71 

JOHNSON, M.E., SCOTT, D.W., MANNING, T.O., SMITH, C.A., LEWIS, R.M., 

(1981) Pemphigus Foliaceus in the Horse. Equine Practice 3, 40-45 

LAING, J.A., ROTHWELL, T.L.W., PENHALE, W.J., (1992) Pemphigus foliaceus 

in a 2month-old foal. Equine Veterinary Journal 24 (6) 490-491 

MANNING, T.O., (1983) Pemphigus foliaceus. In: Current Therapy in equine 

medicine Ed Robinson NE. Philadelphia, WB Saunders Co. pp. 541-542 

PASCAL, A., SHIEBERT, J. IHRKE, PJ., (March 23 to 26, 1995) Seasonality and 

environmental risk factors for pemphigus foliaceus in animals. A retrospective study 

of 83 cases presented to the veterinary medical teaching hospital, University of 

California Davis from 1976 to 1994. Proceedings of the 11 th Annual Meeting of the 

American Academy of Veterinary Dermatology/American College of Veterinary 

Dermatology, Santa Fe, New Mexico, USA pp. 24-25 

SCOTT, D.W., (1989) Autoimmune Skin Diseases in the Horse. Equine Practice 11, 

20-32 

SCOTT, D.W. & Miller, W.H. (2003) Immune mediated Disorders. In: Equine 

Dermatology. Eds WB Saunders Co. Philadelphia. pp. 475- 547 

SCOTT, D.W., WALTON, D.K., SMITH, C.A., LEWIS, R.M., (1984) Pitfalls in 

immunofluorecscence testing in Dermatology. III. Pemphigus-like antibodies in the 

horse and direct immunofluorescence testing in equine dermatophilosis, Cornell 

Veterinarian 74, 305- 311 

98 


SCOTT, D.W., WALON, D.K., SLATER, M.R., SMITH, C.A. and LEWIS, R.M. 

(1987) Immune mediated dermatosis in domestic animals: ten years after. 

Compendium on Continuing Education for the Practicing Veterinarian 9, 424-435 

VANDENABEELE, S.I.J., WHITE, S.D., AFFOLTER, V.K., IHRKE, P.J. (2004) 

Pemphigus foliaceus in Horses: A retrospective study of 20 cases. Veterinary 


VON TSCHARNER, C., KUNKLE G., YAGER, J., (2000) Stannard’s illustrated 

equine dermatology notes. Veterinary Dermatology 11, 172- 175 

WHITE, S.L., (1992) Bullous Autoimmune skin disease: diagnostics, therapy 

prognosis. Proceedings American Association for Equine Practice 28, 507 

YAEGER, J.A., SCOTT, D.W., (1993) The skin and appendages. In: Pathology of 

Domestic Animals IV. Vol I. Ed Jubb, K.V.F. New York, Academic Press. p. 531 

ZABEL, S., MUELLER, R.S., FIESELER, K.V., BETTENAY, S.V., 

LITTLEWOOD, J.D., WAGNER, R. Pemphigus foliaceus in the horse and pony – 

a retrospective study of 15 cases. Veterinary Record, in press. 


Introduction 

100 

How I treat: equine phycomycosis 


Reg Pascoe 

Chronic, subcutaneous, fungal, ulcerative, granulomatous, subtropical and tropical 

skin disease caused by Pythium insidiosum. Affects horses of all breeds, ages and sexes. 

Most cases occur in summer and autumn Other names include Bursatee, Florida 

horse leech, Swamp cancer.(Bridges & Emmons 1961, Blackford 1984 Scott & Miller 

2003) 


Caused by Pythium spp., free-living aquatic organisms which are not true fungi. Horses 

become infected by standing for long periods in stagnant water with rotting organic 

material and high ambient temperatures. 30º C to 40º C favour infection. Damaged 

skin assists the entry of the organisms into the horse’s skin 


There is no age, sex or breed predeliction. Pruritus occurs early in the infection with 

biting and kicking at affected area with subsequent ulceration of skin or wound 

Most lesions occur on legs and lower abdomen and chest. Lesions are usually single 

and unilateral but occasionally are multiple. Body lesions are often roughly circular 

with a sticky, serosanguineous, stringy discharge which either mats hairs or hangs 

from body wall in thick mucopurulent strands. Numerous irregular, gritty,coral like 

bodies (kunkers) occur within the necrotic sinuses found in the lesion. These are 

composed of fungal hyphae and tissue debris. Involvement of joint and tendons with 

sinus formation is a serious complication. Bone involvement is seldom seen in 

lesions less than four weeks old. Chronically affected horses may show invasion of 

underlying bone commonest areas are the cannon bones sesamoids and phalanges 

Lymphadenopathy occurs in chronic cases 


Sarcoid, habronema infestation in wounds, neoplasms (especially sarcoids and 

squamous cell carcinomas), Mycetoma, Botryomycosis, excess granulation tissue, 

foreign body granulomas and other Zygomycetes.

Diagnosis 

History of access of horses to water-logged pasture or lagoon creeks, or inescapable 

rain flooded paddocks. 

Clinical signs of pruritus with serosanguineous stringy discharge is almost 

pathognomonic. 

Biopsy early lesions; send fresh sample for culture and culture immediately on 

selective media such as Campy blood agar or on Sabouraud's dextrose agar (if being 

transported for over 1 to 3 days, samples are better transported on ice packs and 

cultured on non-selective blood agar) (Grooters et al 2002). 

Histopathology 

Cytological examination of aspirates and direct smears shows granulomatous and 

pyogranulomatous inflammation with possible eosinophils. Fungal elements are 

often found in foci of necrotic material (kunkers) , Such findings are not definitive 

due to the similarity to the hyphae of Basidiobolus haptosporus and Conidiobolus coronatus 

Management 

There are no reported cases of spontaneous remission with pythiosis. 

Surgical excision of the tumour is the most common and successful method, 

particularly in the more chronic cases. As the surgery can be both extensive and time 

consuming, general anaesthesia is usually preferred (Bridges & Emmons 1961, 

Bridges 1972, Restrepo et al 1980). 

Surgery on leg lesions is considerably aided if tourniquets are used above the surgical 

area. Careful dissection over tendon and joint locations is important and in some 

cases, close application of tumour to joint capsule and tendon sheath makes the 

surgical approach extremely difficult. Due to the extensive nature of the draining 

holes and sinus, the skin edges often cannot be closed. 

Strong iodine is packed into the surgical area and pressure bandages are applied to 

the lesion. These are left in situ for 2-3 days, and once granulation has commenced, 

the wound can be left unbandaged. Local application of strong iodine (10%) may 

have some beneficial effect. Repeat surgery is more usual than not when the lesions 

occur around tendons and joints. 

Intravenous medication with sodium iodide, 1g/15kg b.w. twice at weekly intervals 

(Pascoe 1973) is a useful adjunct to surgery, and also aids in the reduction of some 

abdominal growths of excessive size. Amphotericin B was used both systemically 

and topically (McMullan et al 1977). Intravenous treatment was well tolerated at an 

average daily dose starting at 0.38 mg/kg and increasing to as high as 1.47 mg/kg. 


They concluded that ideal treatment would be early surgical removal of the lesion, 

followed by daily intravenous and topical administration of Amphotericin B, with 

periodical extirpation of small necrotic tracts as necessary. Cost and a fairly high risk 

of nephrotoxicity due to Amphotericin B may be a deterring factor and more 

recently some strains of Pythium have shown resistance to amphotericin B (Eaton 

1993).More recent information has cast serious doubt on the efficacy of parentral 

Amphoteracin B and parentral treatment is now questionable 

Local treatment: 

After surgical removal of the tumour, Amphotericin B (50g Amphotericin B in 10ml 

sterile water) + 10ml DMSO in gauze was applied and bandaged in place. Treatment 

is continued daily for at least 1 week. 

More recently a severe case involving bone lesions in a mare was treated by surgery 

followed by daily packing with Ketaconazole, Rifampin, DMSO and 2N HCI applied 

to the wound cavity under bandages pre-coated with 10% Povidone-iodine ointment 

to stop leaking of the initial dressing. Immunotherapy was used as an adjunct to 

treatment in this case (Eaton 1993). 

Originally the production of a phenolised vaccine manufactured by the 

department of Tropical Veterinary Science, Townsville, showed indications of 

success in the treatment of early lesions. Results of vaccination compare favourably 

with surgery and when used in conjunction with surgery, has given very good results. 

This is given in 2ml doses weekly for 2-6 weeks. Lesions show some regressions in 

7-10 days after the first injection, but reaction at the injection site can be moderate to 

severe. Indications of successful treatment are reduction of pruritus, drying of 

exudate, expulsion of 'kunkers', fibrosis of granuloma and eventually, complete 

epithelialization (Miller 1981). 

Recently two types of vaccines were produced (Newton & Ross 1993), one being 

that originally developed in 1981 by Miller who produced a vaccine prepared with 

killed sonicated whole-cell hypha antigen of P. insidiosum. 

A second vaccine prepared by precipitation of soluble antigen from Pythium growth 

medium showed a similar cure rate with less side effects at the injection site and 

reportedly has a longer shelf life (Mendoza et al 1992). Successful treatment depends 

on a number of factors such as the age of the horse, general physical condition, 

previous treatment, age/size/site of the lesion and whether there is bony 

involvement. Young fresh lesions of 2 weeks duration responded very well to 

immunotherapy alone, but if present for more than 2 months, there was a poor 

response to this treatment (Mendoza et al 1992). 

Horses with infection in the bone have mostly died, even though they have some 

clinical improvement with surgery and post-operative medical treatment (Alfaro & 

Mendoza 1990). 

102 


These vaccines are not manufactured commercially at this time, but may be available 

on request from select diagnostic laboratories 

Prognosis 

Good for body wall lesions. Guarded for lesions involving joints and tendon. 


Basidiobolus haptosporus 

Introduction 

A member of Zygomycetes, a soil saprophyte, causing lesions on chest, abdomen, head 

and neck. A similar disease to Pythiosis with several important clinical differences. 

Aetiology/Pathophysiology 

Characteristically this disease occurs in a much drier environment than Pythium, 

usually in dusty conditions. Lives in the soil. Injury allows entry to horse’s body. 

Single lesions are common 


As for Pythiosis but growths are more shallow, are confined to neck and abdomen 

with no isolations on legs. Kunkers are small to non-existent. Pruritus is moderate to 

severe 


Pythiosis, mycetoma exuberant granulation tissue, habronema infestation, neoplasms, 

fibroblastic sarcoids. 

Diagnosis 

As for Pythiosis infection. Occurs in drier conditions and organisms probably live in 

soil. "Kunkers" are smaller and few in number. Fungal hyphae found in foci of 

necrosis. 

Biopsy: culture punch samples direct into Sabouraud’s dextrose agar. 

Management 

Surgery is curative if all affected tissue is removed. Sodium iodide 1g/15kg b.w. 

given intravenously twice weekly as a 3.5% solution in normal Sodium chloride 

solution. No vaccine is available. 

Prognosis 

Guarded to good. 

104 


References 

Alfaro AA & Mendoza L (1990) - Four cases of equine bone lesions caused by 

Pythium insidiosum; Equine vet J 22(4):295-297 

Blackford J (1984) - Superficial and deep mycosis in horses; Vet Clinics Nth Am 

LargeAnimal Practice 6:1 

Bridges CH & Emmons CW (1961) - A Phycomycosis of Horses caused by 

Hypomyces destruens; J Am vet med Ass 138:579 

Eaton SA (1993) - Osseous involvement by Pythium insidiosum. Compend Contin 

Educ Pract 15(3) 485-488 

Grooters AM et al (2002) Evaluation of microbial culture techniques for the 

isolation of Pythium insidiosum from equine tissues: J Vet Diag Invest 14 288 

McMullan WC, Joyce JR, Henselka DV & Heitmann JM (1977) - Amphotericin B 

for the treatment of localised subcutaneous Phycomycosis in the horse: J Am vet 

med Ass 170:1293 

Mendoza L, Villalobos J, Calleja CE et al (1992) - Evaluation of two vaccines for the 

treatment of Pythium insidiosum in horses; Mycopathologia 119:89-95 

Miller RI (1981) - Treatment of equine Phycomycosis by immunotherapy and 

surgery Aust vet J 57:377-382 

Newton JC& Ross PS (1993) Equine pythiosis: an overviewof immunotherapy 

Comp Cont Educ Prac Vet 15:491 

Pascoe RR (1973) The nature and treatment of skin conditions observed in horses in 

Queensland Aust vet J 49:35-40 


Philadelphia PA . USA 

Restrepo LF, Morales LF, Robledo M, Restrepo A, Tenica C & Correa de I (1973) - 

Antioquia Medica 23:13-25, cited by RI Miller (1980) Treatment of Equine 

Phycomycosis by Immunotherapy and Surgery; Aust vet J 57:377-382 


106 

How I treat: equine dermatophytosis 

Introduction: 


Greg Burton 

Dermatophytes are a group of septate fungi that invade keratinised tissues (skin, hair 

and nails). The infectious stage is the arthroconidia (arthrospores). Arthrospores are 

released from hyphal fragmentation and have been reported to remain viable in 

environs for up to 12 months. Dermatophytic fungi of the genera Microsporum and 

Trichophyton have been isolated from equine cases of dermatophytosis including, 

M. canis, M. equinum, M. gypseum, * T. equinum, T. equinum var autotrophicum, 

T. verrucosum and T. metagrophytes var. mentagrophytes. A number of other 

species are also isolated in rare cases. 

* T. equinum is the most commonly isolated dermatophyte in horses 

Pathogenesis: 

Clinical lesions seen in dermatophytosis will vary depending on the virulence of the 

dermatophyte and the immunological response of the host. Young horses (< 2 years) 

and immunocompromised horses may have increased susceptibility. Infection occurs 

via direct or indirect contact with arthrospores in epithelial debris. Arthrospores 

adhere to keratinised tissue and germinate within 6 hours. Trauma to the skin (tack 

rub, arthropods, scratching) and warmth and wetting of the skin (sweating, 

macroclimate) can facilitate germination. Race tracks and horse studs provide 

grouped, working horses that combined with the right climatic conditions can create 

an ideal situation for rapid spread of dermatophytes. 

The incubation period post inoculation has been reported as 7 to 42 days. 

Dermatophytes produce keratinases to assist penetration into the hair cuticle and 

grow downward in the follicle until they reach the keratogenous zone. Active keratin 

production (growing hairs) is needed to maintain the infection within the follicle. 

Large numbers of arthrospores are produced and spread to neighboring follicles. 

Centrifugal growth gives the characteristic annular appearance to the lesion. 

Experimentally T. equinum infections will continue to enlarge for 3 to 10 weeks and 

heal within 5 to 14 weeks. 

As with any infectious disease the host’s response to the pathogen plays a major role 

in determining the clinical lesions. Inflammatory changes in the skin may be induced

y a variety of fungal metabolites. T equinum produces urease, gelatinase, protease, 

hemolysins, keratinases and lipases. Trichophyton spp 

have been shown to produce proteolytic enzymes capable of inducing acantholysis. 

As well as pro-inflammatory metabolites T. mentagrophytes produces mannans that 

may inhibit T cell responses and reduce epidermal turnover (exfoliation being an 

innate defence mechanism of the skin to surface microbes). Concurrent bacterial 

infection is sometimes seen in dermatophytosis and dermatophytes may liberate 

penicillin-like substances that result in the formation of penicillin resistant bacteria 

from affected skin. 

There seems to be a lack of specific immunological studies in the equine however 

based on other species it would appear that spontaneous resolution is associated 

with the development of cell mediated immunity (IFNγ and IL2). There does not 

appear to be any correlation with antibody titres. Recovered horses from T equinum 

and M. gypseum infections are reported to be resistant to re-infection with 

dermatophytes of the same species. 


Dermatophytosis is a follicular infection so the common clinical symptom is of 

folliculitis. This may include hive like follicular tufts, annular, peripherally expanding 

areas of alopecia with variable scaling or crusting, classical ring lesion with peripheral 

papules, coalescing areas forming serpiginous patterns of alopecia, exudative lesions 

on the caudal fetlocks “grease heal” and rarely subcutaneous and dermal nodules 

(dermatophytic pseudomycetoma). Pruritus is minimal or absent unless complicated 

by ectoparasites and pain is uncommon unless complicated by Staphylococcal 

folliculitis. 

Lesions in dermatophytosis are most commonly seen on the face, neck, dorsolateral 

thorax and the girth area. It has been reported that dermatophytosis affecting the 

girth is most likely to be T equinum (fomite transmission) and that M. gypseum is most 

commonly isolated from face, neck, legs and rump (geophylic fungus spread via 

arthropods). T verrucosum is reported to have a thicker, grayish crust. Due to clinical 

overlap, lesion type and location should not be relied on to identify species of 

dermatophyte involved. 

Zoonotic factors: 

T equinum, T. verrucosum and M. canis all have zoonotic potential 

Differential diagnoses: 

Other folliculitides 

- Staphylococcal folliculitis 

- Dermatophilosis 

- Pemphigus foliaceous 

- Eosinophilic folliculitis 


Dermatophytic pseudomycetoma requires differentiation from other infectious and 

inflammatory granulomas and neoplasia. 

Diagnosis: 

History 

- Affected in-contact animals or people 

- Duration and progression of the lesion 

Diagnostic tests 

- Wood’s lamp of limited value in the horse 

- Trichogram to identify hyphae and arthrospores, sensitivity of 54 to 64% 

- Acetate tape looking for hyphae 

- Pustule cytology (acantholytic form) 

- Culture, standard dermatophyte test media of limited use (specific culture 

requirements needed for some species) 

- Histopathology and PAS stains 

Treatment: 

Spontaneous remission usually occurs in healthy horses within 12 weeks. Treatments 

are aimed at shortening the duration of the lesions in the infected horse, reducing 

the discomfort associated with the inflammation and restriction of transmission to 

other animals. 

Step 1. 

108 

- Isolation of infected horses 

- Identify and control concurrent health, environmental and nutritional 

issues 

- Reduce work load on horse 

Step 2. 

- Topical antifungals 

- Systemic antifungal therapy? 

- Antibiotic therapy? 

Step 3. 

- Environmental decontamination 


Authors recommendations: 

1. Both Imaverol ® (0.2% enilconazole rinse) and Malaseb ® (2% chlorhexidine 

2% miconazole, Dermcare Vet) appear effective at reducing the duration of 

disease. I am happy to use either and recommend weekly to twice weekly whole 

body treatments 

2. I also recommend the use of Lamisil ® ointment (terbinafine) to individual 

lesions where practical twice daily 

3. I do not recommend the use of systemic antifungals in horses with 

dermatophytosis 

4. I find concurrent bacterial folliculitis uncommon with the exception of disease 

involving the lower limbs. This generally responds to Trimidine powder 15 to 

30mg/kg bid for 3 to 4 weeks. 

5. I have no personal experience with dermatophytic pseudomycetoma but the 

literature suggests these lesions are usually singular and surgery is curative. 

Environmental decontamination: 

1. Washable surfaces, tack, blankets grooming equipment should be treated with 

0.2% enilconazole twice at 10 day intervals. 

2. Tack, grooming equipment should not be shared with other horses. 

3. Straw, bedding materials that are not treatable should be destroyed. 

Prophylaxis 

1. Recovered animals are unlikely to be infected again. 

2. Attenuated live and inactivated T. equinum vaccines have been used in Europe 

and the USA respectively. Vaccines were administered intramuscularly on two 

occasions, 14 days apart. Both vaccines were effective at preventing or reducing 

the severity of disease with both experimental and naturally occurring challenges. 

Points for discussion. 

1. IDEXX laboratories report zero equine dermatophyte cultures in the last 18 

months. Is identifying the species important? 

2. Topically applied porphyrins followed by UVA therapy has been shown to be 

effective in human dermatophytosis. This may support the anecdotal reports that 

equine dermatophytosis resolves more rapidly in sunny conditions. 

3. Trichophyton spp antigens have been demonstrated to cause IgE mediated 

reactions in humans with asthma and clinical severity of asthma has been 

reduced with antifungal therapy. Any role for antifungal therapy in COPD in 

horses? 


How I treat: equine chorioptic mange 

110 



Equine chorioptic mange is caused by the surface-living mange mite Chorioptes bovis 

var equi. Mites are principally found on the lower limbs of horses with feathered 

lower limbs, causing variable irritation and erythema, alopecia, exudation and 

crusting, although some infested animals may show only seborrhoea. Although leg 

mange is the usual clinical manifestation, infestation of the body may also occur. 

Clinical signs and mite numbers are higher in winter months, with mites thriving in 

groups of stabled horses and also surviving for prolonged periods off the host, in the 

presence of epidermal debris, and dark, humid and cool conditions. 

There are no licensed products for this disease in the United Kingdom, necessitating 

the use of drugs off label, according to the “cascade” guidance on prescribing. There 

are a number of options open to the clinician, with varying amounts of evidence in 

support of each. 

Flumethrin is licensed for bovine chorioptic mange in Eire and mainland Europe 

and is available as a sheep scab and tick product in the UK; the 6% solution can be 

diluted 1:900 and applied at a dose rate of 30ml/kg, repeated in 14 days. 

Doramectin, eprinomectin and moxidectin have claims for bovine chorioptic mange 

in the USA. However, clinicians in the USA often use ivermectin at 0.3mg/kg per os 

weekly on 4 occasions. 

A published clinical trial with oral ivermectin paste given orally at the dose of 

0.1mg/kg per os daily for 7-10 days or 0.2mg/kg twice at 2 week intervals, 

eliminated mites in 74% of treated horses, with only occasional mites in the 

remaining animals, whereas large numbers of mites remained in the control group 

(Littlewood et al 1995). 

Topical 2% lime sulfur washes are also used in the US, weekly for up to 6 

applications. A pilot study using 1% selenium sulphide shampoo was effective in 

treating 7 infested horses. Whole body washes were given on three occasions at 5 

day intervals; the hair was clipped from the limbs of two of the horses (Curtis 1998). 

The author has previously shown that chlorhexidine bathing had no curative effect 

in infested horses, although it assisted in controlling secondary bacterial infection. 

On the basis that fipronil is effective for a similar disease in dogs, cheyletiellosis, as 

well as for harvest mite infestation, 0.25% fipronil spray was used to treat a case of

chorioptic mange by the author (Littlewood 2000). A single application was 

successful in securing parasitic cure and resolution of all clinical signs. Subsequent to 

this a blinded, randomised, controlled clinical trial was undertaken in a group of 

army horses with an endemic problem of leg mange. The lower limbs of infested 

horses were sprayed with either 0.25% fipronil spray or isopropyl alcohol vehicle, at 

a dose rate of 500ml per horse. Parasitological cure was achieved in all the horses in 

the verum group, but in none of the horses in the placebo group, after only a single 

application. (Littlewood 2001). Epidemiological work undertaken alongside this 

study revealed that horses may be subclinically affected. On the basis of this work 

the author's current recommendation is that all horses in contact with diseased 

patients, in addition to the clinically affected animals, should be treated and the 

environment should be thoroughly cleaned. 

In addition to the above options, many UK equine clinicians are using injections of 

moxidectin, with anecdotal success and no reactions that have been reported to the 

author, and it is likely that a controlled trial may be undertaken in the near future. 

References: 

Curtis C F (1999) Pilot study to investigate the efficacy of a 1% selenium sulphide 

shampoo in the treatment of equine chorioptic mange. Veterinary Record 144, 674-675 

Littlewood J D (2000) Chorioptic mange; successful treatment with fipronil. Equine 

Veterinary Education 12, 144-146 

Littlewood J D (2001) Equine chorioptic mange: an epidemiological study and 

controlled clinical trial. RCVS Diploma Dissertation 

Littlewood JD, Rose JF & Paterson S (1995) Oral ivermectin paste for the treatment 

of chorioptic mange in horses. Veterinary Record 137, 661-663 


Introduction 

112 

How I treat: equine vasculitis 


Linda Vogelnest 

Vasculitis is an uncommon disease in the horse that most frequently affects the skin, 

however may affect multiple body organs. Cutaneous vasculitis can occur in a variety 

of clinical forms and is characterised by lesions of purpura, urticarial wheals, or 

necrosis and ulceration. Similarly to cutaneous vasculitis in other animals and 

humans, disease aetiology and pathogenesis are complex and incompletely 

understood. A diverse range of triggering primary aetiological events underlies this 

disease in humans, including inflammatory, autoimmune and malignant diseases, 

although ~50% cases remain idiopathic. In the horse, clearly identified aetiological 

agents include bacterial infections (Streptococcus equi or zooepidemicus [“strangles”], 

Salmonella spp., and Corynebacterium pseudotuberculosis); and viral infections (equine 

influenza and equine viral arteritis). Drugs (eg phenylbutazone, vaccines), immunemediated 

colitis, cholangiohepatitis, omphalitis in foals, photo-activation, and 

neoplasia have also been implicated in disease aetiology, however many cases of 

equine cutaneous vasculitis remain idiopathic. 

Disease Pathogenesis 

Both immunological and non-immunological mechanisms have been implicated in 

disease pathogenesis; however immune-complex deposition and damage to small 

vessels, most often postcapillary venules, is reportedly the most common mechanism 

in humans and of proposed importance in animals. A complex series of events 

leading to disease may include initial antigenic stimulation, local immune complex 

deposition & inflammatory-mediator release (TNF-α, IFN-γ, IL-1, IL-4, IL-8), 

complement activation, increased local endothelial cell adhesion molecule expression 

(LFA-1, ICAM-1, E-selectin, P-selectin), coagulation (enhanced by plasminogen 

activator inhibior-1 [PAI-1]), and immunological response to initial inflammation (eg 

dermal dendritic cells, LH cells and T cells) further enhancing inflammation. 

Disruption to blood flow in affected vessels may result from inflammatory cell attack 

of vessel walls (which may be neutrophilic, lymphocytic or rarely eosinophilic or 

granulomatous, classically resulting in leukocytoclastic changes), inflammatory 

mediator damage to endothelial cells (producing primarily hyalinisation), or 

thrombogenic or hypercoagulable states (where thrombosis predominates).

Clinical Disease 

The clinical result of disruption to blood supply from cutaneous vasculitis is lesions 

that range in severity from wheals, papules, purpura, erythema and oedema if acute; 

to alopecia and scarring if mild and chronic; to areas of well-demarcated necrosis, 

ulceration and crusting if severe. Lesions occur most commonly on the distal limbs, 

pinnae, lips and periocular areas. Diascopy confirms purpura as erythemic lesions 

that will not blanch. Signs of systemic illness, including pyrexia, lethargy, decreased 

appetite and weight loss may accompany cutaneous lesions. Forms of cutaneous 

vasculitis recognised in horses include: 

1. Purpura Haemorrhagica - is reported as the most common form of 

cutaneous vasculitis in the horse. It is an acute disease characterised by extensive 

oedematous swelling of the distal limbs, ventral abdomen, and sometimes face and 

muzzle, and typically concurrent signs of systemic illness. Incidence is low and 

sporadic, with most affected horses greater than 2 years of age, and no apparent 

breed or sex predispositions. This syndrome may occur within 2-4 weeks of a 

respiratory infection (Streptococcus equi or zooepidemicus), or other potential triggering 

factors or disease. Urticaria may occur initially, and progress to oedema that is 

usually well-demarcated, painful, symmetrical, and involving all four limbs. Severely 

affected areas may have surface serum exudation and progress to necrosis and 

ulceration. Petechiae and ecchymoses may be present on mucous membranes. Most 

affected horses have obvious signs of depression and are reluctant to move, 

anorexic, tachycardic, tachypnoeic, and often pyrexic. There is a wide variation in 

severity and clinical course. 

2. Subacute Pastern Vasculitis – is proposed to be a relatively common 

although poorly characterised entity in the horse. Lesions primarily occur on nonpigmented 

lower limbs, and may be more prevalent in animals on pasture. Sunlight 

exposure and photactivation are proposed aetiological factors in some cases, 

however appear uninvolved in others. Early lesions include erythema and 

oedematous swelling, which progress to serum exudation, necrosis, crusting and 

ulceration. Pain on palpation is often present, and pruritus absent. Chronic lesions 

may be alopecic, scaling, lichenified, and proliferative. 

Diagnosis 

Definitive diagnosis of cutaneous vasculitis requires consistent history, clinical 

lesions, and histopathological changes. In acute disease varying degrees of specific 

vessel wall changes may be identified, including disproportionately more leukocytes 

within vessel walls than surrounding perivascular areas, leukocytoclasis within or 

adjacent to walls, fibrinoid necrosis, and vessel thrombosis. Less specific supportive 

changes include intense oedema, red cell extravasation, and endothelial cell swelling. 

There may be evidence of cutaneous infarction if severe, and follicular atrophy 

(“faded follicles”) with chronic disease. Clear histological support for a diagnosis of 


cutaneous vasculitis can be difficult to obtain, and similarly to other dynamic disease 

processes, multiple and repeat biopsies may be needed to confirm a diagnosis. 

Treatment 

Aggressive treatment for cutaneous vasculitis is indicated in severe disease to prevent 

extensive ulceration and limit tissue damage and scarring. Glucocorticoids are the 

cornerstone of therapy for severe cutaneous vasculitis in humans, with prednisolone 

considered the most reliable medication for reducing lesions and halting progression 

of disease. Similarly, prednisolone is widely used for treatment of equine cutaneous 

vasculitis, with oral doses of 2-4mg/kg once daily reported successful. In more 

recalcitrant cases, dexamethasone 0.2-0.4mg/kg once daily may be more effective at 

inducing response. Daily induction doses should be continued until the disease is in 

clinical remission and then gradually reduced, with alternate day dosing commenced 

as soon as possible. With severe or slowly responsive cases, reduction in dose by 

25% of the 48-hour dose per 10-14 days has been recommended to help limit 

relapse. Such high-dose glucocorticoid therapy should ideally be instituted 

concurrently with a management plan to minimise the risk of laminitis, as 

glucocorticoids, in particular triamcinolone or dexamethasone have been linked to an 

increased risk of this debilitating disease. Low energy diets, weight control, and 

regular gentle exercise are strongly recommended. In the acute stages of cutaneous 

vasculitis supportive care including hydrotherapy, walking and good skin hygiene can 

also be helpful. 

The clinical course of cutaneous vasculitis in any patient is difficult to predict, with 

some cases resolving completely within a few weeks, and others becoming chronic 

or recurrent. It is important to search thoroughly for underlying aetiological factors, 

especially in severe, chronic or recurrent cases, and treat promptly wherever possible. 

Minimising factors likely to exacerbate vasculitis, such as excessive stress, heat or 

cold exposure is also proposed of help with human disease. The use of alternative 

immunomodulating drugs to glucocorticoids for equine cutaneous vasculitis appears 

unreported, however a range of other drugs have been used in human disease. For 

treatment of severe, chronic, or poorly responsive cutaneous vasculitis in humans, 

azathioprine, cyclophosphamide, methotrexate, or mycophenolate mofetil have been 

recommended. Little or no information is available on the use of these drugs in the 

horse, however expense likely limits their use regardless. For subacute and chronic 

disease in humans, drugs including colchicine, dapsone, sulphasalazine, and 

antimalarial agents can be effective alternatives or additions to prednisolone. 

Colchicine and dapsone primarily inhibit neutrophil chemotaxis and activation, so 

are theoretically most likely to be effective in neutrophilic vasculitis. Dapsone or 

sulphasalazine are reported to be effective steroid-sparing options in some forms of 

canine cutaneous vasculitis. The author has used Dapsone in one horse with initial 

urticaria progressing to purpura haemorrhagica syndrome, at a dose of 1mg/kg twice 

daily for over 4 weeks concurrently with prednisolone. There was apparent poor 

response, with continued rapid relapse on attempts to lower prednisolone dosage. In 

cutaneous vasculitis in humans caused primarily by thrombosis some further 

114 


treatment options have been used. Pentoxifylline, that modifies plasticity of red 

blood cells allowing easier passage through narrowed vessel lumina, along with a 

myriad of inhibitory effects on cytokines, leukocytes and endothelial cells, is an 

apparently safe and well-tolerated option with efficacy in both human and canine 

disease, although a lag phase of weeks to months to see beneficial effects is apparent 

in humans. Low-dose aspirin, anabolic steroids, anticoagulants, and 

niacinamide/tetracycline combinations have also been used. 

In summary, for acute cutaneous vasculitis in the horse, rapid treatment with 

prednisolone at immunosuppressive doses is currently the recommended treatment 

option. A search for underlying aetiological factors is vital, and a concurrent 

management plan to minimise risks of laminitis prudent, along with general 

supportive and wound care to help limit the debilitation of severe disease. For 

recalcitrant or recurrent cases with poor response or glucocorticoid side-effects, 

alternative options remain speculative, with little information available on efficacy or 

safety. More potent glucocorticoids such as dexamethasone or triamcinolone may be 

used to help induce remission in severe cases. Dapsone has been used in a steroidsparing 

role in at least one horse without evidence of benefit at the doses and 

duration chosen, but also without apparent adverse effects, and it may be used as a 

treatment option for poorly responsive or subacute disease. Screening for adverse 

haematopoietic or liver effects, which have been reported in humans with the use of 

this drug, may be indicated. Pentoxifylline has been used safely in the horse, and 

could similarly be considered for poorly responsive or subacute disease, especially if 

there is histological evidence of vessel thrombosis in the face of minimal 

inflammation. Gold salts are another option to consider for recalcitrant disease and 

have been used effectively and safely in horses with pemphigus foliaceus and some 

other immune-mediated diseases, although their use in equine vasculitis appears 

unreported, and they are not a recognised treatment option for cutaneous vasculitis 

in humans. 

References 

Equine Dermatology. Scott DW. WB Saunders, St. Louis, Mo. 2003: 522-546. 

Cutaneous Vasculitis Update. Gibson LE. Dermatologic Clinics 2001:19;4:603-615. 

Purpura haemorrhagica in 53 horses. Pusterla N, Watson JL, Affolter VK et al. 

Veterinary Record 2003. 153: 4, 118-121. 


116 

Notes 


Notes 


118 

Notes

here - Australian College of Veterinary Scientists

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